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PubMed1992

Maternal T cells of immunized pregnant mice induce immune suppression in their offspring.

The present study focused on the influence of maternal immunity during pregnancy on the responsiveness of the immune system(s) in offspring. Maternal immunization of pregnant mice with T-dependent foreign antigen sheep red blood cells (SRBC) induced suppression of anti-SRBC plaque-forming cell (PFC) responses in their offspring. We attempted to identify the cell species among the maternal lymphoid cells of the immunized pregnant mice that induced this suppression in their offspring, by separating the maternal cells into T cells, B cells and macrophages, or T-cell subsets, and then adoptively transferring them into other normal pregnant mice. The results demonstrated the following: first, maternal CD4+ T cells of immunized pregnant mice induced immune suppression in their offspring. Second, maternal T cells could be activated during pregnancy in the same fashion as in non-pregnant mice. The T-cell factor(s) for the immune suppression in offspring is produced not only by maternal T cells of immunized pregnant mice but also by T cells activated in non-pregnant mice. Third, cellular organization was required for maternal T cells to induce this immune suppression in their offspring.

Animals↗

PubMed2003

[Influence of immunization dose schemes on the immune response to anti-tetrodotoxin vaccine].

OBJECTIVE: To study the relationship between the immune response of anti-tetrodotoxin vaccine, including its dose-response, and to select optimal immunization dose so as to enhance antitoxic effect of the anti-tetrodotoxin vaccine. METHODS: Tetrodotoxin (TTX) was coupled to Tachypleus tridentatus hemocyanin (TTH) chemically to form artificial antigen (TTX-TTH), and with which Balb/c mice were immunized. Influence of different immunization doses [100 microg as the higher (H) and 25 microg as the lower (L) dose group] on the protective effects of TTX vaccine was compared. The quality of antisera and effects of vaccine in anti-TTX poisoning were observed. RESULTS: The sera antibody quality increased more quickly in group L than that in group H after immunization. The dose at which the half of immunized mice survived when challenged once with TTX were 16 x LD (1 LD = 13.5 microg/kg, i.p.) in group L and 11 x LD in group H. When TTX was used time and again, the half of immunized mice could tolerate as high as 40 x LD and 22 x LD of accumulated dose, and the maximum tolerable cumulated dose was 104 x LD and 90 x LD for group L and H respectively. The scheme L was better both in antibody quality and effect of protecting against TTX toxicity than that in scheme H. CONCLUSIONS: The experimental vaccine of TTX could effectively protect animal from TTX intoxication. The lower immunization dose in this study is selected as the optimal immunization scheme.

Animals↗

PubMed2005

Immunization of mice with crude extract of Saccharomyces boulardii yeast induces cross-reactive immune responses with antigenic preparations from different developmental stages of the Schistosoma mansoni and reduces the parasite worm burden.

Immunization of mice with Saccharomyces boulardii crude extract caused a significant reduction in Schistosoma mansoni worm burden (23.7%; P = 0.02) in comparison to control mice. Mice sera collected after the 1st immunization showed a significant increase (P < 0.05) in both IgM and IgG against parasite soluble cercarial antigenic preparation (CAP) than unimmunized mice sera (UMS). Upon 2nd immunization, sera from yeast extract immunized mice (YIM) showed increase of IgM and IgG (1.6 and 1 fold) against CAP than UMS. Sera collected 2, 4 and 6 weeks (W) after infection of YIM with S. mansoni cercariae showed higher IgM (1.4, 1.5 and 1 folds) and IgG (0.9, 1.2 and 1.1 folds) levels against CAP than sera of infected UM (IUM). When compared to sera from UM, a week post 1st and 2nd immunization sera showed a significant elevation (P < 0.05) of both IgM and IgG to parasite soluble adult worm antigenic preparation (SWAP). Sera collected at 2, 4 and 6W after infection of YIM with parasite cercariae showed higher IgM (1.1, 1.3 and 1.2 folds) and IgG (1.2, 1.1 and 1.3 folds) reactivities against SWAP than sera of IUM. One week post 1st and 2nd immunization with the yeast extract, sera showed a significant increase (P < 0.05) of both IgM and IgG levels against parasite soluble egg antigen (SEA) when compared with sera from UM. At 2 and 4W post infection, sera from immunized infected mice showed a significant decrease in IgM (P < 0.05) but the decrease of IgG (0.7 fold) was not significant when compared to IUM. Six weeks post infection the decrease in both antibodies remained but it was significant for IgG (P < 0.05) but not for IgM (2.1 folds) when compared with IUM. Immunization with S. boulardii extract caused a non-significant increase (1.2 folds) in mesenteric lymph node (MLN)-CD4+T cells, significant elevation of MLN-CD8+T cells (P < 0.05) and a non-significant increase (0.9 folds) of B-cells when compared to that of UM. Also, Immunization with S. boulardii extract caused 1 fold elevation in both CD4+ and CD8(+)-T lymphocytes in thymus of YIM when compared with their counts in thymus of UM.

Animals↗

PubMed2006

[The role of Toll-like receptors (TLR) in innate and adaptive immune responses and their function in immune response regulation].

The innate immune response is a universal mechanism of host defense against infection. It functions on the basis of special receptors called PRRs (pattern-recognition receptors) which recognize conserved microbial structures called PAMPs (pathogen-associated molecular patterns). Due to PRRs, the human organism is able to discriminate between self and non-self antigens. Toll-like receptors (TLRs) are a group of PRRs that play a crucial role in "danger" recognition and the induction of immune response. Cells of the immune system (macrophages, dendritic cells, mast cells, eosinophils, neutrophils, B lymphocytes), epithelial cells, endothelium, cardio-myocytes and adipocytes all recognize pathogens via TLRs. TLR stimulation via microbial products activates the innate immune response. This results in an upregulated synthesis of anti-bacterial substances and pro-inflammatory cytokines as well as the activation of dendritic cell maturation (increased expression of co-stimulatory molecules and MHC antigens), thereby becoming more effective in antigen presentation. In some cases, the innate immune response is not able to eliminate infection and requires the induction of the adaptive immune response. When activated via TLRs, antigen-presenting cells (APCs) release elevated levels of pro-inflammatory cytokines (TNF-alpha, IL-1, IL-6, IL-8, and IL-12), chemokines, and nitric oxide (NO) and show increased expression of co-stimulatory molecules (CD40, CD80, CD86). All these changes in APC function allow the induction of the adaptive immune response, where both T and B lymphocytes play a crucial role. TLRs also play a role in the regulation of immune response via direct or indirect influence on the function of CD4+ CD25+ T regulatory cells (Tregs), which results in their induction and subsequent suppression of the immune response or a reversal of suppression (contrasuppression).

Adaptation, Physiological↗

PubMed1990

Secretory immune responses in mouse vaginal fluid after pelvic, parenteral or vaginal immunization.

Intravaginal immunization causes IgA responses in vaginal fluid, but so far lymphoid nodules in mouse vaginal mucosa have not been detected. The present study was therefore designed to test the hypothesis that IgA responses in the female reproductive tract may be generated in the regional iliac lymph nodes. Two, non-mucosal sites were identified in the female mouse pelvis, the subserous and presacral spaces, from which lymph drains mainly to the iliac nodes. Immunization at these pelvic sites with horse ferritin adsorbed to aluminum hydroxide (AH) caused much higher IgA and IgG titres in vaginal fluid than intravaginal immunization; moreover, the pelvic immunizations caused significantly higher and better sustained IgA titres in vaginal fluid than subcutaneous immunization near the scapulae or in the perineum, while IgG titres in vaginal fluid were similar in these groups. Additional mice were immunized with ferritin subcutaneously near the scapulae or in the presacral pelvic space using dimethyl dioctadecyl ammonium bromide (DDA), AH plus muramyl dipeptide, or the Ribi adjuvant system as adjuvants. Pelvic immunization caused higher IgA titres in vaginal fluid than subcutaneous immunization in each case. The IgA response stimulated by DDA was similar to that produced by AH but higher than the responses caused by the other two adjuvants, while IgG titres were similar with all four adjuvants in both sites. The results suggest that non-mucosal, pelvic immunization is particularly effective in stimulating IgA responses in the female reproductive tract. The observation is consistent with the possibility that the iliac lymph nodes may play a role in the development of IgA responses in the reproductive tract.

Adjuvants, Immunologic↗

PubMed1989

Systemic immune response to oral polio immunization in patients with IgA nephropathy.

The systemic immune response to a booster dose of attenuated polio vaccine has been studied in a group of patients with IgA nephropathy, their parents and healthy unrelated controls. The serum IgA and IgG antibody response and the antibody response in cultured lymphocyte supernatants was quantitated by a sensitive radio-immunoassay. Three of eight patients and two of their parents had elevated serum IgA antibody to polio pre-immunization. There was no significant rise in serum IgA or IgG antibody to polio post-immunization in any group. However, the five subjects with elevated pre-immunization levels fell into the normal range post-immunization, suggesting IgA specific suppression. Total and antigen specific IgA rose post-immunization in culture supernatants in all groups. The rise did not differ among the groups. The patients and parents with high serum antibody also had high culture supernatant levels and these fell post-immunization. There was an increased antigen non-specific IgG response in four patients and three of their parents. The data provide additional in vivo evidence of an upregulated IgA immune response in patients with IgA nephropathy. In addition, the data provide the first in vivo evidence of aberrant immune responses in the first degree relatives of patients with IgA nephropathy. This appears to be one of perhaps several inherited traits which may predispose an individual to develop this common and progressive nephropathy.

Administration, Oral↗

PubMed1984

Squamous-cell carcinoma, Kaposi's sarcoma and Burkitt's lymphoma are consequences of impaired immune surveillance of ubiquitous viruses in acquired immune deficiency syndrome, allograft recipients and tropical African patients.

The immune system has evolved under Darwinian pressures as a defence against ubiquitous viruses. Immune surveillance against viral antigens protects the normal host. Individuals with inherited or acquired immune-deficiency disorders can become vulnerable to ubiquitous viruses and neoplasms can ensue, such as B-cell lymphoma, hepatocellular carcinoma, squamous-cell carcinoma, Kaposi's sarcoma, and carcinoma of the penis and uterine cervix. Immunodeficiency permits Epstein-Barr virus, hepatitis B virus, papillomavirus, herpes simplex virus, and cytomegalovirus to induce sustained target-cell proliferation. Each virus selects specific cellular targets bearing viral receptors and the infection leads to proliferation of the target cells rather than lysis. Various co-factors, including nutrition, exposure to tumour-promoting agents, parasitic infection, and ultraviolet light, may promote carcinogenesis. Depending on the type and severity of the immune deficiency, gradual proliferation may lead to evolution of a malignant clone. Conversion of polyclonal virally infected proliferating cells to give monoclonal malignancy is probably due to specific cytogenetic rearrangements which allow oncogene activation and endow an altered tumour cell with selective growth advantages over normal diploid cells. Prevention of viral oncogenesis may be possible by treatment of immune-deficient individuals with premalignant disorders. Immunotherapy and antiviral therapy may prevent progression of viral-induced proliferation to malignancy. The purpose of this paper is to discuss and evaluate the role of immune deficiency and viruses in the induction of malignancies commonly occurring in Africans residing in sub-Saharan Africa (Purtilo, 1976). The types of malignancies commonly occurring in this region are believed to be due to ubiquitous viruses. A failure of immune surveillance mechanisms to recognize viral antigens and abrogate proliferation of infected target cells predisposes to malignancy by increasing the chance of a proliferating cell undergoing a cytogenetic or molecular alteration which endows it with malignant characteristics. The immunological surveillance hypothesis has been elaborated during this century by Ehrlich, Thomas, Burnet, and Schwartz (reviewed by Purtilo & Linder, 1983). This hypothesis rests on several assumptions: that neoplastic cells possess unique tumour antigens: tumour antigens provoke an immune response in the host; and the immune response is protective and eliminates the tumour.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗

PubMed1995

Paradoxical IgA immunity in CD4-deficient mice. Lack of cholera toxin-specific protective immunity despite normal gut mucosal IgA differentiation.

Using normal and CD4 gene-targeted (CD4-/-) mice, we asked whether mucosal immune responses and IgA B cell differentiation require the presence of CD4+ T helper cells. We found that CD4-/- mice had numerous B cell germinal centers in Peyer's patches and other gut-associated lymphoid tissues. Membrane IgA+ B cells were found to co-localize to germinal center areas and CD4-CD8- double negative CD3+ T cells had replaced CD4+ T cells in the follicular areas of the Peyer's patches. CD4-/- mice had normal levels of IgA-producing cells in gut-associated lymphoid tissues, and gut lavage contained unaltered levels of total IgA. However, despite T cell help for IgA B cell differentiation, CD4-/- mice did not respond with Ag-specific intestinal IgA following oral immunization with the powerful mucosal immunogen cholera toxin (CT). By contrast, these mice demonstrated serum alpha-CT IgG following oral immunization, suggesting that double negative CD3+ T cells provided some help for systemic immune responses after oral immunization. Perorally immunized CD4-/- mice were completely unprotected against CT-induced diarrhea while both normal and CD8-/- mice were well protected and also demonstrated high levels of gut mucosal alpha-CT IgA. After reconstitution of the CD4-/- mice by adoptive transfer of naive mesenteric lymph node CD4+ T cells, the mice acquired the ability to respond with specific mucosal immune responses following oral immunization and also developed resistance against CT-induced diarrhea. Thus, paradoxically, although IgA B cell differentiation appears to proceed normally in CD4-/- mice, specific gut mucosal immune responses are grossly impaired in the absence of CD4+ T cells.

Animals↗

PubMed1996

Spinal cord NMDA receptors modulate peripheral immune responses and spinal cord c-fos expression after immune challenge in rats subjected to unilateral mononeuropathy.

To characterize further the neural involvement in local immune reactions, we evaluated the effect of intrathecal NMDA-receptor blocker dizocilpine maleate (MK-801) on the peripheral immune response itself and on spinal cord c-fos expression induced by the delayed-type hypersensitivity (DTH) response. Immune challenge took place in the hind paw ipsilateral or contralateral to an injured sciatic nerve in both previously sensitized and immune-naive animals. An enhanced immune response was observed bilaterally in the hind paws of animals subjected to unilateral mononeuropathy compared with sham-operated controls. In contrast, no such enhancement was observed when neuropathic animals were challenged in the front paws. The increased DTH response was blocked successfully by the intrathecal administration of an analgesic dose of MK-801. Compared with sham-operated animals, animals subjected to unilateral mononeuropathy showed both a differential distribution and an increase in the number of c-fos-labeled neurons in the dorsal horn of the L3-L5 spinal cord segments after immune challenge. This was observed irrespective of whether the challenge took place ipsilateral or contralateral to the injured nerve. In addition to reversing the changes in immune response, intrathecal administration of MK-801 reversed the pattern of c-fos immunoreactivity in the spinal cord after immune challenge in neuropathic animals. These data suggest that select groups of spinal cord neurons participate in enhancing the peripheral immune response to a specific antigen in neuropathic animals and that this enhancement involves central NMDA receptors.

Animals↗

PubMed1997

Complete protective immunity induced in mice by immunization with the 19-kilodalton carboxyl-terminal fragment of the merozoite surface protein-1 (MSP1[19]) of Plasmodium yoelii expressed in Saccharomyces cerevisiae: correlation of protection with antigen-specific antibody titer, but not with effector CD4+ T cells.

The 19-kDa carboxyl-terminal fragment of the merozoite surface protein-1 (MSP1) is a leading malaria vaccine candidate but is unable to induce immunity in all monkeys or all strains of mice. The mechanism of immunity is unclear, although data show that cell-mediated immunity plays a critical role following immunization with the larger mature MSP1 protein. We optimized a vaccine protocol using the MSP1(19) fragment of Plasmodium yoelii expressed in Saccharomyces cerevisiae, such that following exposure of mice to parasites, they remained undetectable in peripheral blood, whereas control animals all died at very high parasitemia within 10 days. We then depleted the vaccinated mice of >99% of CD4+ T cells by anti-CD4 mAb treatment and could show that infections in most animals remained subpatent following challenge. Furthermore, mice in which the gene for the mu-chain of Ig had been disrupted could not be immunized with MSP1(19). Immunity in normal mice did not depend on the presence of an intact spleen nor production of nitric oxide, persisting unabated when >70% of splenic macrophages were depleted. Thus, while effector CD4+ T cells may contribute to immunity, neither they nor factors associated with a Th1-type cell mediated immune response appeared to play the major role in MSP1(19)-induced protection in normal mice. Furthermore, T cells were not sufficient for immunity in mice lacking B cells. In normal mice, protection correlated with a very high titer of MSP1(19)-specific Abs (>6,400,000), predominantly G1 and G2b, which may function by merozoite neutralization.

Animals↗

PubMed2000

Induction and maintenance of immune effector cells in the gastric tissue of mice orally immunized to Helicobacter pylori requires salivary glands.

BACKGROUND & AIMS: Helicobactor pylori mostly colonizes the gastric mucus that contains salivary antibodies. We studied the role of saliva in the induction and maintenance of gastric immunity conferred by oral vaccination against H. pylori. METHODS: C57BL/6 mice underwent a sialoadenectomy before and after intragastric immunization using whole-cell sonicates of H. pylori and cholera toxin as an adjuvant. At 1 and 6 months after oral inoculation, we assessed the density of the H. pylori colonizing the stomach, specific antibodies in gastric secretion and sera, and the constituents of cellular infiltrates in the tissue. RESULTS: A sialoadenectomy before, but not after, immunization abrogated protection by the vaccination at 1 month after inoculation. Protected mice had more neutrophils, plasma cells, and lymphocytes, but fewer eosinophils, in the gastric tissue than nonprotected mice. Protected mice had a greater increase of immunoglobulin (Ig) G1 specific to H. pylori than IgG2a in sera. At 6 months after inoculation, oral immunization was less effective in mice who had a sialoadenectomy than in control immunized mice. The antibody titers in both gastric secretion and in sera did not correlate with the density of bacteria colonizing the stomach. CONCLUSIONS: It is suggested that, in intragastric immunization against H. pylori, saliva is necessary for both the induction and maintenance of optimal immunity in the stomach. Effective immunity was associated with an increased number of neutrophils and lymphocytes in gastric tissue.

Administration, Oral↗

PubMed2005

Dissection of antigen-specific humoral and cellular immune responses for the development of experimental immune-mediated blepharoconjunctivitis in C57BL/6 mice.

PURPOSE: Allergic conjunctivitis is characterized by allergen-specific IgE in the serum and infiltration of eosinophils into the conjunctiva. However, it remains unclear whether early-phase reaction (EPR) mediated by Ag-specific IgE links to late-phase reaction (LPR) in the conjunctiva. We aimed to investigate whether LPR is mediated by either cellular or humoral immune responses. METHODS: Experimental immune-mediated blepharoconjunctivitis (EC) was induced in C57BL/6 mice by either active immunization or passive immunization by transfer of ragweed (RW)-primed lymphocytes and RW-specific IgE, followed by RW challenge onto the conjunctiva. Transferring RW-primed lymphocytes were prepared from RW-primed splenocytes which were stimulated in vitro with RW for 3 days. Fifteen minutes after RW challenge, clinical findings were evaluated and 24 hr after challenge, the conjunctivas and sera were harvested for histologic analysis and measurement of IgE, respectively. RESULTS: EPR was most prominent when EC was induced by transfer of RW-specific IgE. EPR was hardly detectable if EC was induced by transfer of RW-primed lymphocytes. Mild EPR was noted when EC was induced by active immunization. LPR, evaluated by infiltration of eosinophils into the conjunctiva, was most severe when EC was induced by transfer of RW-primed lymphocytes. Minimal, but definite LPR was induced when EC was induced by transfer of RW-specific IgE. Intermediate severity of LPR was induced when EC was induced by active immunization. CONCLUSIONS: LPR in the conjunctiva is dominantly mediated by cellular immune responses, whereas EPR in the conjunctiva is putatively mediated by humoral immune responses. Importantly, LPR in the conjunctiva is inducible by Ag-specific IgE alone, although minute.

Allergens↗

PubMed1975

Immune mechanisms in leukemia: suppression of cellular immunity by starvation.

The effects of starvation on the cellular immune response of C58/Wm mice to syngeneic malignant lymphoid cells (1b cells) were studied. Mice were starved 1-3 days before or after immunization. The capacity of starved animals to survive immunization was used to quantify immunosuppression. When starvation bracketed immunization by -1 to +1 days, only 2 of 23 mice survived primary immunization, compared with 100% survival for nonstarved controls. A 2-day period of starvation +1 to +7 days after primary immunization reduced survival about 30%. For a test of the effect of starvation on the secondary immune response, mice were immunized, starved 2 days, and then challenged with viable lb cells. When mice were starved from -3 to +1 days before or after challenge, there was a 25-45% decrease in survival. Starvation caused a disproportionate depletion of lymphoid tissue elements. The proportional loss in the weight of the spleen and thymus was essentially twice as great as the loss in total body weight. The peripheral blood leukocyte count was reduced by about 20% when mice were starved 1 day and by approximately 50% when they were starved 2 days. When mice were starved 1-2 days, the differential leukocyte count did not shift and there was no significant change in the number of blood erythrocytes or in the hematocrit. Starvation for 2 days caused a 65-70% reduction in the number of viable mononuclear spleen cells. Starvation for 3 days caused about 90% reduction. Adoptive cell transfer experiments showed that the immunocompetence of individual spleen immunocytes was not reduced by starvation.

Animals↗

PubMed1979

Local cholera immunity in mice: intestinal antitoxin-containing cells and their correlation with protective immunity.

Methods for light and electron microscopic identification and characterization of intestinal cholera antitoxin-containing cells (ACC) using peroxidase-labeled immunoreagent are described and used to study the ACC response in mice after immunizations with cholera toxin. Specific ACC appeared in significant numbers after two oral immunizations and increased six- to eightfold with two additional oral boosters, whereas further oral immunizations caused no additional stimulation. Intravenous immunizations had to be repeated seven times before ACC could be detected. After two oral immunizations, most of the ACC were found in the proximal part of the small intestine and no ACC were seen in the colon. This uneven distribution of ACC within the small intestine was eliminated after four oral immunizations, when ACC could also be detected in the colon. The ACC response after four oral immunizations demonstrated a peak at 4 days with far fewer cells present at 2 and 7 days. Electron microscopic studies showed that the ACC were mature plasma cells with the staining localized to the endoplasmic reticulum. Regression analysis of the relationship between the number of ACC and the magnitude of protective immunity against intestinal challenge with cholera toxin indicates a highly significant correlation (r = 0.91, P less than 0.001).

Animals↗

PubMed1973

Immunity to Vibrio cholerae in the mouse. II. Effect of a cell-adherent immune factor.

Serum, peritoneal exudate cells, or spleen cells were obtained from donor mice immunized with Vibrio cholerae Ogawa 41. Normal recipients were protected from lethal Vibrio infection when challenged one day after transfer of immune serum or peritoneal cells or normal peritoneal cells exposed in vitro to immune serum. Protection of recipients of immune spleen cells was evident when the cell transfer-challenge interval was 14 days but not when it was 1 day. Transfer of immunity with peritoneal cells from actively immunized donors was long lasting, whereas that derived from in vitro treatment of normal cells was of short duration. Both a cell-adherent and a nonadhering immune factor appear to be important in this immunity.

Animals↗

PubMed1976

Immune processes in the course of infection with dysentery bacilli. I. Transfer of immunity by means of spleen cells.

Studies on the mechanisms of immune phenomena in the course of infections with dysentery bacilli in mice showed that injection of live Shigella sonnei phase I bacilli intravenously evokes the appearance in the spleen of cells by means of which immunity to a lethal dose of these microorganisms can be transferred into other mice. Immunity to a lethal dose of the bacteria was measured by the number of animals surviving the infection, and by the numbers of bacteria isolated from the organs of the animals. "Active" cells appeared in the spleen 4-8 days after immunization. Spleen cells obtained from mice earlier than 4-8 days after immunization, or from non-immunized mice, were inactive. The role of cell-mediated immunity, reactivity to endotoxins per se, and specific immunoglobulins in immunity to bacterial dysentery in mice are discussed.

Animals↗

PubMed1994

Improved cell-mediated immune responses in HIV-1-infected asymptomatic individuals after immunization with envelope glycoprotein gp160.

Strong specific T-cell responses to human immunodeficiency virus type 1 (HIV-1) gp160 were induced by immunization with recombinant gp160 (rgp160). It was given as postinfection vaccination to 40 asymptomatic HIV-1 seropositive patients. The participants received 6 doses of 160 micrograms rgp160 administered intramuscularly at 0, 1, 4, 8, 17, and 26 weeks and were monitored for 1 year. Lymphocyte proliferation was performed by cultivating lymphoid cells in vitro with specific antigens and mitogens. After immunization with gp160, specific T-cell proliferative responses were induced in all 40 patients. One week after the sixth immunization at day 180, a substantially increased response was detected in 98% of the patients, with a mean stimulation index value of 195. Furthermore, proliferative responses were also identified, after immunization, against native gp120 and against a peptide representing the V3 region of gp120. In addition to the HIV-specific T-cell responses, increased reactivity to several other non-HIV antigens, including tetanus toxoid, influenza, measles, and cytomegalovirus, were seen after gp160 vaccination. The responses to CMV and measles were interpreted to represent an improved recall antigen response. Such recall antigen responses were few in matched HIV-infected controls immunized with influenza virus only. All patients initially and repeatedly showed a normal capacity of total T-cell activation, evaluated by the mitogen phytohemagglutinin (PHA). The trend in CD4 counts improved in 30 of 40 patients during the year of follow-up. The frequency of increases of proliferative responses to antigens was associated with a better CD4 trend. Addition of zidovudine for 2 weeks after each immunization had no beneficial effects nor did it prevent induction of immune responses. All patients tolerated the immunizations well, and no systemic adverse effects were noted. This is a phase I trial, and no definitive conclusions regarding clinical efficacy can be reached.

Adult↗

PubMed1996

Immune dysfunction in Down's syndrome: primary immune deficiency or early senescence of the immune system?

Multiple immunologic disturbances are commonly observed in individuals with Down's syndrome including abnormal proportions of peripheral blood lymphoid subsets, cellular dysfunction, and autoimmune phenomena. However, a majority of the individuals with this syndrome do not show clear features of immunological disease. Many of these immunological alterations are age-related changes and can be enclosed in the spectrum of multiple signs of early senescence characteristic of Down's syndrome.

Aging↗