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PubMed1982

Formation and clearance of tubulointerstitial immune complexes in kidney of rats immunized with heterologous antisera to Tamm-Horsfall protein.

Tubulointerstitial immune complex nephritis was produced by passive immunization of rats with antisera to rat Tamm-Horsfall protein (TH), a surface membrane glycoprotein of the cells of the thick ascending limb of Henle's loop. Circulating anti-TH antibodies were deposited in the kidney after an intravenous injection of rabbit antisera to TH. These anti-TH antibodies combined with TH at the base of tubular cells in the thick ascending limb of Henle's loop and formed granular immune complexes in situ in the space between basal cell surface membranes and tubular basement membranes. Immune complexes were also selectively formed in this site during perfusion of isolated kidneys with antisera to TH. Tubular immune complexes containing immunoglobulin, complement, and TH were maximal during the first week after an intravenous injection while high circulating anti-TH antibody titers were present. As the antibody titers subsequently fell to undetectable levels, tubular immune complexes were rapidly cleared and were virtually absent 4 weeks after the injection. During this clearance phase, rabbit IgG and rat TH were detected in the renal interstitium and in renal hilar lymph nodes. The rapid clearance of subepithelial TH immune complexes contrasts with the prolonged persistance of both glomerular subepithelial immune complexes and basement membrane deposits formed after injection of heterologous antisera to other renal components. The process of rapid clearance of tubulointerstitial immune complexes may allow rapid reversibility of immune injury in tubulointerstitial nephritis.

Animals↗

PubMed2001

Induction of immune hyporesponsiveness after portal vein immunization with ovalbumin.

BACKGROUND: Previous work has demonstrated prolonged allograft survival after donor-specific portal vein immunization before the transplantation. The purpose of this study was to examine the potential mechanism of portal vein-induced hyporesponsiveness after portal vein immunization with the soluble protein ovalbumin. METHODS: Balb/c mice were immunized with a portal vein injection of ovalbumin. After the immunization, in vivo delayed-type hypersensitivity response and in vitro proliferative response of ovalbumin-specific T cells were assessed to determine host immune response. Type 1 (IL-2, IL-12, IFN-gamma) and type 2 (IL-4, TGF-beta) regulatory cytokines were assessed by semiquantitative reverse transcriptase polymerase chain reaction. Sera anti-ovalbumin IgG, IgG1, and IgG2a were measured by enzyme-linked immunosorbent assay, and the antigen-presenting ability of liver nonparenchymal cells (NPCs) was assessed by T-cell proliferation to ovalbumin in vitro. RESULTS: There was significant inhibition of ovalbumin-specific delayed-type hypersensitivity and T-cell proliferation in portal vein-immunized mice compared with intraperitoneal-immunized or control mice. Reverse transcriptase polymerase chain reaction analysis results showed that lymphocytes from portal vein-immunized mice exhibited decreased type 1 and increased type 2 cytokine messenger RNA expression compared with intraperitoneal-immunized or control animals. The type 2 cytokine response of lymphocytes from ovalbumin portal vein-immunized mice correlated with increased sera ovalbumin-IgG1 and decreased IgG2a. The results of an antigen-presenting assay revealed that liver NPCs were deficient antigen-presenting cells compared with adherent cells from heart or spleen. CONCLUSIONS: Processing of ovalbumin by hepatic NPCs results in hyporesponsiveness to ovalbumin by an impaired type 1 cytokine response and a preferential shift toward a type 2 cytokine response, possibly because of defective antigen presentation by hepatic NPCs. Intrahepatic processing of antigen may play an important role in the development of strategies to reduce host immunoreactivity against transplanted allografts.

Animals↗

PubMed1971

Specific immune response genes of the guinea pig. II. Relationship between the poly-L-lysine gene and the genes controlling immune responsiveness to copolymers of L-glutamic acid and L-alanine and L-glutamic acid and L-tyrosine in random-bred Hartley guinea pigs.

The ability of guinea pigs to make immune responses to GA, a linear random copolymer of L-glutamic acid and L-alanine, GT, a random linear copolymer of L-glutamic acid and L-tyrosine, and PLL, a linear homopolymer of L-lysine, is controlled by different autosomal dominant genes specific for each of those polymers. We have investigated the relationship between the PLL gene and the GA and GT immune response genes by simultaneously immunizing random-bred Hartley strain guinea pigs with GA and PLL, GT and PLL, or GA and GT. In most Hartley guinea pigs the ability to respond immunologically to GA and to PLL is inherited together; that is, most animals responding to GA respond to PLL and vice versa. However, a few animals respond to either GA or to PLL but not both, demonstrating that the GA and PLL immune response genes are not identical but linked in most Hartley animals. Conversely, when simultaneously immunized with GT and PLL, most Hartley guinea pigs respond to either PLL or GT but not both, indicating that GT and PLL responsiveness tends to segregate away from each other. Thus, the GT and PLL immune response genes also are not inherited independently but, rather, behave as alleles or pseudoalleles. Similar results are observed when Hartley guinea pigs are simultaneously immunized with GA and GT. The ability to respond to GA segregates away from the ability to respond to GT. Our studies demonstrated that the specific immune response genes thus far identified in guinea pigs controlling the ability to respond to GA, GT, and PLL, respectively, are found on the same chromosome. In most Hartley animals, the GA and PLL immune response genes are often linked, i.e. occur on the same chromosome strand, and tend to behave as alleles or pseudoalleles to the GT immune response gene.

Alanine↗

PubMed2006

Functional roles of immature dendritic cells in impaired immunity of solid tumour and their targeted strategies for provoking tumour immunity.

Dendritic cells play a crucial role in initiating tumour immunity as well as in the immune response for invading foreign pathogens such as bacteria and viruses. For bacterial and viral infections, the immature dendritic cells (iDCs) residing in peripheral tissues are efficiently activated and matured by pathogen signals for performing the immune response. In contrast, for self-antigens, the naive T cells are not activated by iDCs but proceed to anergy/deletion, and the generation of regulatory T cells for immune tolerance. The induction of immune response and tolerance is regulated strictly by iDCs as the sensor for homeostasis of immune response in the host. Despite the identification of some tumour antigens, tumour immunity is not provoked successfully. Even though there are some critical obstacles to inhibit effective tumour immunity, tumour cells are able to exploit the functional roles of iDCs for tumour progression, which are induced by tumour-derived soluble factors such as vascular endothelial growth factor (VEGF) and functionally modulated in the microenvironment. The iDCs still remain as the critical target for provoking tumour immunity. In this review, the functional roles of tumour-associated iDCs and the strategy for targeting iDCs in effective tumour immunity for the cancer patient are discussed.

Autoantigens↗

PubMed1989

Impaired immune responsiveness in Plasmodium berghei immune mice.

Mice immunized against Plasmodium berghei parasites by drug-controlled infection exhibited decreased immunoresponsiveness against rabbit red blood cells (RRBC). Increasing RRBC antigen dose increased responsiveness, but agglutinating anti-RRBC antibodies of the IgG class remained undetectable. Clearance of colloidal carbon from the bloodstream of malaria-immunized mice was not different from controls. Removal of all the persistent parasites from immune mice did not restore responsiveness until 140 days after treatment, suggesting that the parasite per se did not influence responsiveness directly. Because of this, and because of the fact that priming of mice with RRBC before P. berghei immunization was not more effective than priming after immunization, it was concluded that antigen uptake and subsequent presentation were not impaired in P. berghei immune mice, in contrast to infected mice. Anti-RRBC antibodies were detected in serum of P. berghei immune mice, but regulation of responsiveness to RRBC by transfer of such immune mouse serum was not found. Immunoglobulin levels, especially of the IgG2 and IgG3 subclass were elevated in sera of P. berghei immune mice, which indicated an LPS-like polyclonal activation. The results also suggest that during drug-controlled infection, which leads to immunity against infection, a state of B-cell tolerance is induced.

Animals↗

PubMed2005

Enhanced breadth of CD4 T-cell immunity by DNA prime and adenovirus boost immunization to human immunodeficiency virus Env and Gag immunogens.

A variety of gene-based vaccination approaches have been used to enhance the immune response to viral pathogens. Among them, the ability to perform heterologous immunization by priming with DNA and boosting with replication-defective adenoviral (ADV) vectors encoding foreign antigens has proven particularly effective in eliciting enhanced cellular and humoral immunity compared to either agent alone. Because adenoviral vector immunization alone can elicit substantial cellular and humoral immune responses in a shorter period of time, we asked whether the immune response induced by the prime-boost immunization was different from adenoviral vaccines with respect to the potency and breadth of T-cell recognition. While DNA/ADV immunization stimulated the CD8 response, it was directed to the same epitopes in Gag and Env immunogens of human immunodeficiency virus as DNA or ADV alone. In contrast, the CD4 response to these immunogens diversified after DNA/ADV immunization compared to each vector alone. These findings suggest that the diversity of the CD4 immune response is increased by DNA/ADV prime-boost vaccination and that these components work synergistically to enhance T-cell epitope recognition.

AIDS Vaccines↗

PubMed1983

Transplacental immunization of the human fetus to tetanus by immunization of the mother.

Experimental studies in rats showed that immunization of the pregnant female led to the transplacental immunization of her fetuses. The possibility that this also occurred in humans was explored by immunizing 42 pregnant women with tetanus toxoid (2.5 or 5 Lf) in the fifth and eighth months of pregnancy and comparing the immune responses of their offspring with the responses of the offspring of 25 unimmunized mothers. Only the offspring of the immunized mothers were sensitized to tetanus. IgM antitetanus antibodies were in their blood before immunization with diphtheria, pertussis, tetanus vaccine (DPT), they had a more rapid (P less than 0.01) response to DPT immunization, and they were still highly sensitized (P less than 0.01) to tetanus 13 mo after birth. In addition, pregnancy had no immunosuppressive effect (P less than 0.05) on the responses of the mothers to tetanus toxoid. Thus, transplacental immunization occurs in humans; it enhances the response of the offspring to subsequent immunization, and it could be used to circumvent the necessity for immunization in early neonatal life.

Adolescent↗

PubMed1989

Immune, growth and carcass responses of ram lambs to active immunization against desulfated cholecystokinin (CCK-8).

This study explored feed intake and carcass responses to active immunization against desulfated cholecystokinin-octapeptide (CCK-8) in ram lambs. Antibody titers 8 wk following primary immunization and booster immunizations given at 4 and 6 wk averaged greater than 1:1,000. Titers increased to greater than 1:10,000 by 16 wk following a final booster immunization at 11 wk. The antibodies developed against desulfated CCK-8 exhibited 29% and 13% cross-reactivities for sulfated CCK-8 and gastrin-17, respectively. Immunization against desulfated CCK-8 had no effect on feed intake, ADG, carcass weight or carcass quality grade. Backfat thickness and carcass yield grade were reduced (P less than .05) by immunization. Organ weights at slaughter, including those of the pancreas and small intestines, were not affected by CCK-8 immunization, with the exception of the lungs, which were 16% lighter (P less than .01) in immunized lambs. In conclusion, active immunization against desulfated CCK-8 resulted in development of high antibody titers against desulfated and sulfated CCK-8. Immunization against CCK-8 decreased fat content of the carcass but failed to affect feed intake, carcass weight or ADG.

Animals↗

PubMed2000

CD4+ T cells acting independently of antibody contribute to protective immunity to Plasmodium chabaudi infection after apical membrane antigen 1 immunization.

Apical membrane Ag 1 (AMA1) is a leading malaria vaccine candidate. Homologues of AMA1 can induce protection in mice and monkeys, but the mechanism of immunity is not understood. Mice immunized with a refolded, recombinant, Plasmodium chabaudi AMA1 fragment (AMA1B) can withstand subsequent challenge with P. chabaudi adami. Here we show that CD4+ T cell depletion, but not gammadelta T cell depletion, can cause a significant drop in antiparasite immunity in either immunized normal or immunized B cell KO mice. In normal mice, this loss of immunity is not accompanied by a decline in Ab levels. These observations indicate a role for AMA1-specific Ab-independent T cell-mediated immunity. However, the loss of immunity in normal CD4+ T cell-depleted mice is temporary. Furthermore, immunized B cell KO mice cannot survive infection, demonstrating the absolute importance of B cells, and presumably Ab, in AMA1-induced immunity. CD4+ T cells specific for a cryptic conserved epitope on AMA1 can adoptively transfer protection to athymic (nu/nu) mice, the level of which is enhanced by cotransfer of rabbit anti-AMA1-specific antisera. Recipients of rabbit antisera alone do not survive. Some protected recipients of T cells plus antisera do not develop their own AMA 1-specific Ab response, suggesting that AMA 1-specific CMI alone can protect mice. These data are the first to demonstrate the specificity of any protective CMI response in malaria and have important implications for developing a malaria vaccine.

Amino Acid Sequence↗

PubMed2001

Passively acquired antibodies suppress humoral but not cell-mediated immunity in mice immunized with live attenuated respiratory syncytial virus vaccines.

A respiratory syncytial virus (RSV) vaccine will need to be administered by 1 mo of age to protect young infants; therefore, it will need to be effective in the presence of maternally acquired RSV Abs. In the present study, the immunogenicity and efficacy of two live attenuated RSV vaccine candidates of different level of attenuation were evaluated in mice passively immunized with varying quantities of RSV Abs. The replication of the RSV vaccines was suppressed in the lower, but not the upper, respiratory tract of the passively immunized mice. Immunization with either vaccine candidate was highly efficacious against challenge with wild-type RSV in both passively immunized and control mice. Nonetheless, a high level of immunity was seen even in passively/actively immunized animals that failed to develop a humoral immune response, suggesting that T cells mediated the immunity. Depletion of CD4+ and CD8+ T cells in passively/actively immunized and control animals at the time of challenge with wild-type RSV demonstrated that CD4+ and CD8+ T cells made significant independent contributions to the restriction of replication of RSV challenge virus in both the upper and lower respiratory tracts. Although passively acquired serum RSV Abs suppressed the primary systemic and mucosal Ab responses of IgM, IgG, and IgA isotypes, B lymphocytes were nevertheless primed for robust secondary Ab responses. Thus, immunity mediated by CD4+ and CD8+ T cells and Abs can be readily induced in mice by live RSV vaccine candidates in the presence of physiologic levels of RSV neutralizing Abs.

Animals↗

PubMed2002

Requisite elements in vaccine immunity to Blastomyces dermatitidis: plasticity uncovers vaccine potential in immune-deficient hosts.

Understanding fundamental mechanisms of vaccine immunity will allow proper use and optimization of vaccines. Vaccination with a genetically engineered, live, attenuated strain of Blastomyces dermatitidis carrying a targeted deletion at the BAD1 locus confers sterilizing immunity against experimental lethal pulmonary infection. We found in this study that alphabeta T cells are requisite for durable vaccine immunity, whereas other T and B cells are dispensable. In immune-competent animals, CD4(+) T-cell derived cytokines TNF-alpha and IFN-gamma mediate vaccine immunity. Surprisingly, these factors are dispensable in immune-deficient animals, which rely on alternate mechanisms for robust vaccine immunity, yet still require O(2)(-) production rather than generation of NO. Our results clarify the cellular and molecular bases behind the first genetically engineered fungal vaccine. They also illustrate a sharp difference in vaccine mechanisms between immune-competent and immune-deficient hosts, which underscores the plasticity of residual immune elements in compromised hosts, and points to the feasibility of developing vaccines against invasive fungal infection in this fast growing patient population.

Animals↗

PubMed1985

Induction of immunity in mice to Fasciola hepatica with a Fasciola/Schistosoma cross-reactive defined immunity antigen.

The paradox of schistosomiasis is that infection confers immunity to its host, yet immunization with subcellular antigens of the parasite does not, in general, induce protective immunity. Infection or immunization with subcellular antigens of Fasciola hepatica confers high levels of immunity to a challenge infection with another trematode, Schistosoma mansoni. We have isolated by antibody affinity chromatography a Fasciola hepatica/Schistoma mansoni cross-reactive antigen, designated FhSmIII(M), and also have shown that this antigen confers immunity in mice to a challenge infection with S. mansoni. This antigen was compared with a crude F. hepatica worm extract (FhWWE) as to its ability to induce an IgG antibody response in mice, and to determine whether it had a protective effect in mice to a challenge infection with F. hepatica metacercariae. Mice immunized with FhSmIII(M) or FhWWE, and subsequently infected with F. hepatica, developed higher IgG antibody levels to FhSmIII(M), as measured by ELISA, than F. hepatica-infected controls. Mice immunized with FhWWE did not develop significant levels of resistance to challenge with F. hepatica metacercariae. Mice immunized with FhSmIII(M) and infected with F. hepatica metacercariae developed 69%-78% less worms than controls. An F. hepatica/S. mansoni cross-reactive, cross-protective defined immunity antigen confers in mice significant levels of protection to a challenge infection with F. hepatica.

Animals↗

PubMedDate not supplied

[Characteristics of immune response to diphtheria anatoxin in children with different immune status during the second age-scheduled revaccination].

The dynamics of the intensity of specific antidiphtheria immunity after the second age-scheduled revaccination was studied in 129 practically healthy children. The study revealed that the formation of immunity depended on the initial functional state of the immune system before the injection of diphtheria toxoid. Three variants of immune response were determined and the immune status corresponding to each of these variants was characterized. As shown in this study, children with the hyperergic character of immune response were characterized by relatively high initial titers of antitoxin, and the injection of an additional dose of the antigen led to the prolonged state of hyperimmunization with the subsequent decrease of the intensity of immunity by half, registered in the catamnestic observation for 4 years. Children with the hypo- and normoergic variants of immune response were characterized by the most stable immune response to diphtheria toxoid, and during the catamnestic observation they formed the levels of antibody titers 2.5- to 3-fold higher than before immunization. But the protection characteristics in children with the third variant were the lowest among the children under study.

Antibody Formation↗

PubMed1989

The effect of passive immunization on active immunity against Clostridium perfringens type D in lambs.

Lambs in different stages of development of active immunity against Clostridium perfringens type D were treated with partially purified immunoglobulin in an attempt to superimpose a passive immunity on an existing or developing active immunity. Three different studies were undertaken to determine the impact of partial purified immunoglobulins on these vaccinated animals. In 2 of the 3 studies, active immunity was induced by administering the normal routine enterotoxaemia vaccinations and allowing the basic immunity to become established, for a period ranging from 2 weeks for the animals in study 1 and 4 months for those in study 2, before passive immunization with the partially purified immunoglobulins took place. An increase in the epsilon antibody titre occurred in each of the 2 studies after the animals were passively immunized with immunoglobulin, though this increase was not statistically significant (P greater than 0.05). In the 3rd study, when the animals were given the initial vaccination of the Onderstepoort enterotoxaemia oil adjuvant vaccine together with the immunoglobulin, an immediate increase in the epsilon antitoxin titre occurred that was statistically significant (P less than 0.05) 2-14 days after administration. No negative effects were noted on the development of an initial active immunity or an existing active immunity against Clostridium perfringens type D when they were passively immunized with partially purified immunoglobulin.

Animals↗

PubMed1986

Immunogenicity of the Gardner lymphosarcoma for the mice of the strain C3H (H-2k). I. The effect of the 60Co-irradiation of recipients and of the interval between the immunization and transplantation of the tumor on the antitumor resistance of immunized mice.

The C3H (H-2k) mice were immunized by 60Co-irradiation-inactivated Gardner lymphosarcoma (LSG) cells. The degree of resistance of mice with transplanted tumors was determined by difference in survival curves of the immunized and nonimmunized mice. When the tumor was transplanted during 26 weeks after the last of the three immunizing injections the mean survival time of immunized mice was always prolonged over that of nonpretreated controls. The prolongation was not always significant. The slope differences between lines characterizing survival of immunized and nonimmunized groups were statistically significant when the transplantation of the tumor was performed up to the 22nd week following the immunization. A small number of immunized mice which survived 60 days without visible tumors belonged to immunized groups transplanted with the tumor up to 14 weeks after the last immunizing dose. A higher degree of resistance has been achieved in mice given increased number of immunizing injections. Similar effect was observed in mice with impaired antitumor resistance due to immunosuppressive dose of 60Co-irradiation given before the tumor transplantation. Skin grafts taken from resistant mice healed up to unaffected isologous mice as well as it was found in reciprocal transplantation experiments.

Animals↗

PubMed1984

Characterization of tick antigens inducing host immune resistance. I. Immunization of guinea pigs with Amblyomma americanum-derived salivary gland extracts and identification of an important salivary gland protein antigen with guinea pig anti-tick antibodies.

Guinea pigs immunized by subcutaneous injection of an emulsion of incomplete Freund's adjuvant (IFA) containing tick salivary gland extract antigens (SGA) from partially fed female ticks expressed a significant level of tick rejection when challenged 17 days later. This level of tick rejection was similar to animals actively sensitized by tick feeding and challenged at the same time. SGA emulsified with complete Freund's adjuvant (CFA) or administered with saline was ineffective. However, ticks that fed on animals immunized with SGA+IFA or SGA+CFA expressed significant reductions in engorgement weight. SGA was active when prepared with or without protease inhibitors. The minimum effective immunizing dose of SGA was between 100 and 280 micrograms per animal. Extracts made from salivary gland-derived cement material (CA) from partially fed female ticks administered at 50 micrograms in IFA induced levels of tick rejection comparable to animals immunized with 280 micrograms of SGA+IFA. Sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS/PAGE) of 35S- and 125I-radiolabeled SGA and CA extracts immunoprecipitated by guinea pig anti-tick serum that transferred immune resistance demonstrated a unique protein of 20,000 m.w. Serum from animals immunized with SGA+IFA (successful immunization) recognized this same protein, whereas serum from animals immunized with SGA+CFA (unsuccessful immunization) did not. The results of this study suggest that a 20,000 m.w. protein derived from the tick salivary gland may be responsible for the induction and perhaps elicitation of host immune resistance responses to Amblyomma americanum ticks.

Animals↗

PubMed1976

Immune processes in the course of infection with dysentery bacilli. II. Transfer of immunity by means of serum.

The role of antibodies in immunity to intravenous infection with dysentery bacilli was studied in mice. Serum from animals immunized with a single dose of live dysentery bacilli obtained at a varying intervals of time after immunization transferred immunity to other mice infected with lethal doses of the same bacilli. Passive immunity transferred with serum was diffrentiated. Sera obtained 4 to 8 days after immunization of the donors with sublethal doses of live Shigella sonnei phase I bacilli protected lethally infected recipients by inhibiting multiplication of the bacilli in the spleen and liver. Highest protective activity of this type was found in sera obtained 6 days after immunization of the donors. Sera obtained after 11 days and later protected the recipients from death, but only negligibly inhibited growth of the bacilli in the internal organs of the animals. It is suggested that immunity to intravenous infection with dysentery bacilli in mice follows a biphasic course. In the first phase, between days 4 and 8 after immunization, cell-mediated immunity and a specific humoral factor play the main role. In the second phase, specific immunoglobulins of the IgG class afford protection.

Animals↗

PubMed1993

Adoptive transfer of immunity to hepatitis B virus in mice by bone marrow transplantation from immune donors.

Recipients of allogeneic bone marrow transplantation are immunosuppressed as a result of their primary disease and by myeloablative therapy. Such patients are dependent on multiple blood products and are at risk for hepatitis B virus infection. Active immunization against hepatitis B in the immediate pre- and post-transplant periods is ineffective, presumably because of decreased T cell-dependent B-cell responses. This study was designed to evaluate, in a mouse model system, the transfer of immunity against hepatitis B to bone marrow transplant recipients through immunization of bone marrow donors against hepatitis B before transplantation. Bone marrow donor BALB/c mice were immunized with a recombinant hepatitis B vaccine. Seroconversion to HBs antibody occurred within 4 wk of primary immunization, and antibody levels in treated donor mice rose above 300 mIU/ml after a single booster injection. Bone marrow recipient mice, conditioned by sublethal irradiation, were injected intravenously with bone marrow cells obtained from syngeneic HBs antibody-positive immune donors. Antibody was detected in 10% of bone marrow recipients within 30 days of transplantation and in 56% 1 mo after a booster injection that led to a secondary rise in HBs antibody. Adoptive transfer of immunity to hepatitis B also occurred after transplantation of T cell-depleted bone marrow cells from hepatitis B-immune donors, albeit at a lower HBs antibody level. These results indicate that immunity to hepatitis B can be transferred in mice by bone marrow transplantation from hepatitis B-immune donors to immunosuppressed recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗