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Results for “Immunity, Cellular”

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PubMed1982

Induction of cellular immunity to Coccidioides immitis after sensitization with dinitrochlorobenzene.

A patient had progressive disseminated coccidioidomycosis and depressed cellular immunity to Coccidioides immitis. He developed a large nasal coccidioidal lesion that was unresponsive to conventional therapy. Application of dinitrochlorobenzene (DNCB) to the nasal lesion was temporally associated with resolution of the lesion and stabilization of the systemic disease. In addition, DNCB application was followed by signs of cellular immunity to C. immitis. These included development of delayed cutaneous hypersensitivity to coccidioidin, as well as lymphokine production and lymphoproliferative responses to coccidioidin. Similar forms of DNCB immunotherapy may prove useful in other patients with fungal disease and depressed cellular immunity.

Adult↗

PubMed1999

Deficient cellular immunity--finding and fixing the defects.

The critical role of cellular immunity in resistance to infectious diseases is glaringly revealed by life-threatening infections if T cell function is disrupted by an inherited or acquired immunodeficiency. Although treatment has historically focused on infectious complications, understanding of the cellular and molecular basis of immunodeficiency and technologies useful for enhancing cellular immunity have both been rapidly evolving. A new era of molecular and cellular therapy is emerging as approaches to correct abnormal genes, the loss of T cell subpopulations, and aberrant T cell homeostasis make the transition from bench to bedside.

Adoptive Transfer↗

PubMed1990

Humoral and cellular immune response in schistosomiasis pre and post praziquantel therapy.

Humoral and cellular immune response in schistosomiasis was studied pre and post praziquantel therapy. After treatment the mean anti SEA IgM and IgG and anti SWAP IgM levels in all cases showed significant reduction. In patients with high eosinophilic count anti SEA IgE and IgA were statistically decreased. Other specific antibodies showed negligible changes Cellular immune response was not affected.

Adolescent↗

PubMed1993

Role of the systemic cellular immune response in the pathogenesis of Helicobacter pylori-associated duodenal ulcer.

20 patients colonized by H. pylori (9 with duodenal ulcer, 11 with antral gastritis) were examined for the presence of a systemic cellular immune response to H. pylori using an in vitro lymphocyte transformation assay. Infiltration of the antral mucosa by myelomonocytic cells was assessed by immunohistology as a parameter of local cellular immune response. A systemic H. pylori-induced cellular reaction could be demonstrated in 11 patients all of whom showed an intense myelomonocytic infiltration of the antral mucosa. In this group 7 of 9 duodenal ulcers occurred. The findings support the hypothesis, that a specific cellular immune response might be involved in the pathogenesis of H. pylori-associated gastritis and duodenal ulcer. A protective role of systemic cellular immunity to H. pylori seems rather unlikely.

Adult↗

PubMed1983

Suppressive effect of bradykinin to cellular immune responses in vivo and in vitro.

Bradykinin, as well as histamine, one of the mediators in IgE mediated immediate type allergic reactions or acute inflammation, may affect the in vitro and in vivo cell-mediated immune reactions of the immunized animals. It was demonstrated in our present experiment that the appearance of delayed type hypersensitivity (DTH) skin reaction in the immunized guinea pig was remarkably suppressed by treatment of bradykinin or histamine and the suppression of cutaneous DTH by bradykinin was inhibited by H-2 antagonist (burimamide) but not by H-1 receptor blocker (chlorpheniramine). It was also clearly demonstrated that bradykinin suppressed the production of antigen-induced macrophage migration inhibitory factor (MIF) of the immune guinea pig peritoneal exudate cells (PECs) and the production of MIF was blocked by H-2 antagonist (burimamide) or H-2 agonist (tolazolin) but not by H-1 antagonist (chlorpheniramine). Antigen-induced lymphocyte proliferation of the immunized mice, one of the indicators of the cellular immune response, was also suppressed by treatment of bradykinin. These results indicate that bradykinin as well as histamine may have some role in the subsequent expression of cellular immune reactions.

Animals↗

PubMed2003

Prime-boost vaccination with HIV-1 Gag protein and cytosine phosphate guanosine oligodeoxynucleotide, followed by adenovirus, induces sustained and robust humoral and cellular immune responses.

A prophylactic vaccine for HIV-1 will probably require the induction and maintenance of both humoral and cellular immunity. One current strategy to achieve such long term immune responses is a prime-boost vaccination approach using a DNA priming inoculation, followed by recombinant viral boost. In this report we use a novel prime-boost approach in which the priming injections consist of recombinant HIV-1 Gag protein mixed with cytosine phosphate guanosine oligodeoxynucleotide (CpG ODN), followed by recombinant adenoviral boost expressing HIV-1 Gag. Analysis of the immune responses indicates that HIV-1 Gag protein plus CpG ODN immunization alone induces potent humoral as well as Th1 and CD8+ T cell responses. Boosting with recombinant adenovirus strikingly enhances CD8+, but not Th1, T cell responses, resulting in CD8+ T cell responses far greater in magnitude than Th1 responses. Furthermore, the Th1 and CD8+ T cell responses following prime-boost immunization were seen in both lymphoid and peripheral mucosal organs and were sustained over several months. Together, these data suggest a new immunization approach for elicitation of long term humoral and cellular immune responses.

AIDS Vaccines↗

PubMed1977

[Results of cellular immune reaction assessment under 5-fluorocytosine therapy].

In the judgment of cellular immune reactions with the help of LTT, taking into consideration age-specific variations in generalised mycoses negative and decreased results, respectively, are found after testing with PHA, PPD, in the mixed culture and with candidine. After overcoming of the generalisation of fungi the finding normalised. While using metabolites in other clinical pictures always a decrease of the cellular immune reaction is found, under treatment with 5-fluorocytosin in generalised mycoses no decrease of the transformation of lymphocytes is to be observed. Here after successful therapy even an adequate increase is shown. The examinations confirm the opinion that 5-fluorocytosin does not condition an influence on the function of the T-lymphocytes.

Child↗

PubMed2000

[Humoral and cellular immunity in meningitis of various etiology].

The parameters of humoral and cellular immunity were studied in patients with meningitis due to tuberculosis and other diseases. Peripheral blood and spinal fluid were measured in 91 and 76 patients with tuberculous meningitis, in 75 and 59 with purulent meningitis, and in 54 and 33 with serous meningitis, respectively. Comparing assessment of the findings revealed profound changes in the content of T lymphocytes and their subpopulations. With this, impaired cellular immunity appeared not only as changes in the relative count of immuno-complement cells, but in their different functional activity detectable by blast cell formation. Thus, in tuberculous meningitis, 18.11 +/- 0.95% of peripheral lymphocytes and 15.1 +/- 1.2% spinal fluid were exposed to the specific blast cell transformation antigen PPD whereas they were 1.94 +/- 0.3 and 2.4 +/- 0.9% (p < 0.001) and 1.86 +/- 0.28 and 3.1 +/- 0.8% (p < 0.001), respectively. Elevated spinal fluid levels of beta 2-microglobulin and IgE in patients are shown to be a differential diagnostic sign typical of tuberculous meningitis.

Antibody Formation↗

PubMedDate not supplied

Cellular immunity in lobomycosis (keloidal blastomycosis).

The cellular immune response of twelve patients from the Brazilian Amazon basin with lobomycosis were assessed. Delayed skin reaction to bacterial and fungal antigens, skin allograft rejection, and sensitization to dinitrochlorobenzene were studied. Ninety-two percent of the patients were not reactive to dinitrochlorobenzene after sensitization; skin allograft rejection occurred in an average of 17 days. Delayed skin reaction to streptococcal, staphylococcal, trichophytin and candida antigens was negative in the majority of the patients. Reactivity to mycobacterial antigens, however, was very high. The results suggest that patients with lobomycosis are partially cellular immunodeficient.

Aged↗

PubMed1994

Humoral and cellular immune responses to the fimbriae of Porphyromonas gingivalis and their synthetic peptides.

Subcutaneous injection of fimbriae from Porphyromonas gingivalis strain 381 in Freund's incomplete adjuvant (FIA) resulted in an excellent serum anti-fimbrial immunoglobulin G (IgG) response in guinea-pigs and BALB/c mice. Administration of P. gingivalis fimbriae also elicited distinct cellular immune responses to the fimbriae in terms of ear lobe reaction in BALB/c but not in BALB/c nu/nu mice, and of skin reaction in guinea-pigs. When the guinea-pigs were given a semi-synthetic adjuvant GM-53--sodium beta-N-acetylglycosaminyl-(1-->4)-N-acetylmuramyl-L-alanyl-D-isogl utaminyl- (L)-stearoyl-(D)-meso-2, 6-diaminopimelic acid-(D)-amide-D-alanine--and fimbriae in FIA by subcutaneous injection, more enhanced production of serum anti-fimbrial IgG and stronger cellular immune responses were induced in the guinea-pigs than in those given fimbriae alone. Synthetic peptide FP381(202-221), which corresponds to the amino-acid residue numbers 202-221 based on the amino-acid sequence of fimbrilin from P. gingivalis strain 381, elicited humoral and cellular immune responses in guinea-pigs immunised with the fimbriae or FP381(202-221). Furthermore, subcutaneous administration of synthetic peptide FP381(61-80) with GM-53 induced lesser degrees of humoral and cellular immune responses in guinea-pigs than did FP381(202-221). However, when the fimbriae or FP381(61-80) were administered with bovine serum albumin (BSA), markedly elevated levels of specific anti-BSA antibody were seen in the serum of BALB/c mice. These results clearly indicated that fimbriae from P. gingivalis 381 and their oligopeptide segments induced humoral and cellular immune responses and exhibited immuno-adjuvant activities in guinea-pigs and BALB/c mice.

Adjuvants, Immunologic↗

PubMed2000

Priming with Chlamydia trachomatis major outer membrane protein (MOMP) DNA followed by MOMP ISCOM boosting enhances protection and is associated with increased immunoglobulin A and Th1 cellular immune responses.

We previously reported that DNA vaccination was able to elicit cellular immune responses and partial protection against Chlamydia trachomatis infection. However, DNA immunization alone did not generate immune responses or protection as great as that induced by using live organisms. In this study, we evaluated the immunologic effects of a combinational vaccination approach using C. trachomatis mouse pneumonitis (MoPn) major outer membrane protein (MOMP) DNA priming followed by boosting with immune-stimulating complexes (ISCOM) of MOMP protein (MOMP ISCOM) for protection of BALB/c mice against MoPn lung infection. Substantially better protection to challenge infection was observed in mice given combinational vaccination compared with mice given MOMP ISCOM immunization alone, and the protection approximated that induced by live organisms. Enhanced protection was correlated with stronger delayed-type hypersensitivity, higher levels of gamma interferon production, and increased immunoglobulin A antibody responses in lung homogenates. The results indicate that DNA priming followed by ISCOM protein boosting may be useful in designing a fully protective chlamydial vaccine.

Animals↗

PubMed2006

An adaptation of recombinant vaccinia-based ELISPOT and intracellular cytokine staining for a comparative measurement of cellular immune responses in HIV-1 and HIV-2 infections in West Africa.

An efficient and quantitative tool for rapid assessment of human immunodeficiency virus (HIV)-induced cellular immune responses is important for resource-limited settings, such as in sub-Saharan Africa. Modifications are required to previously reported methods for evaluating ex-vivo antigen-specific cellular responses based on direct recombinant vaccinia virus (rVV) stimulation of peripheral blood mononuclear cells (PBMCs) by enzyme linked immunosorbent assay (ELISPOT) and by flow cytometry intracellular cytokine assay (ICA). We made such modifications in order to detect specific responses and compared quantitative cellular immune responses in HIV-1 and HIV-2 infected Gambians. The sensitivity of the rVV-based ELISPOT assay was on average 1.25 interferon (IFN)-gamma spot forming cells (SFC) per 50 000 PBMCs specific for either infection, and 5 IFN-gamma-secreting CD8+ T cells/50 000 in the ICA. The level of IFN-gamma SFC detected by ELISPOT and by ICA were correlated (P < 0.02). ICA detected pol-specific responses in 88% and 67% of HIV-1 and HIV-2 subjects, respectively, and gag-specific responses in more than 80% of both infections. Lower proportions of responders were obtained with ELISPOT, for which pol responses were present in 60% of HIV-1 and 46% of HIV-2 infected patients, and gag responses in 55% and 69%, respectively. The assays did not show any significant difference in cellular immune responses between HIV-1 and HIV-2 infected subjects with CD4% >or= 20%. These outcomes are comparable with results obtained using standard techniques and thus this method is a suitable, rapid and less expensive assessment of cellular immunity.

Adult↗

PubMed1990

Donor-specific cellular immunity in rejecting and long-term-surviving class I-disparate rat renal allograft recipients.

The effects of pre- and posttransplant immunization on graft survival, infiltrate intensity, and host in situ/systemic cellular immune responsiveness were examined for class I MHC-disparate rat renal allograft recipients. Naive, unsensitized PVG (RT1c) recipients of class I MHC disparate PVG.R1 (RT1.Aa on PVG background) orthotopic kidney transplants displayed long-term (greater than 50 days) survival (LTS) in a majority (41/52) of cases. Pretransplant immunization of recipients with a PVG.R1 skin graft most often resulted in rejection (mean survival greater than 21.3 days) with 8/15 rats surviving less than or equal to 2 weeks and only 3/15 with LTS. Pretransplant immunization with a skin graft from a fully MHC-disparate PVG.1A (RT1a on PVG background) donor resulted in acute rejection (mean = 6.1 days) with 0/8 rats surviving greater than or equal to 2 weeks. Donor-specific class I and II disparate (PVG.1A), and third-party (LEW) skin transplants applied on LTS (greater than 50 days) PVG.R1 kidney graft recipients showed typical 1st- and accelerated 2nd-set skin graft rejection, but had no effect on kidney graft survival. In contrast, 6/7 LTS PVG.R1 kidney graft recipients accepted PVG.R1 skin grafts indefinitely following their transient partial rejection. Histologic analysis of kidney allografts revealed the highest degree of mononuclear cell infiltrates in animals specifically sensitized by PVG.1A skin grafts prior to transplant. Donor class I-specific cytotoxic T lymphocyte precursor (pCTL) frequencies, as determined by limiting dilution assays, were increased and equivalent at 1 week posttransplant in kidney allograft cell eluates from nonrejecting naive recipients (1/127-1/2209) and rejecting presensitized animals (1/470-1/7848). LTS animals had decreased intragraft pCTL at greater than 50 days (1/2969-1/61875), as did LTS at greater than 50 days that received PVG.R1, PVG.1A, or LEW skin grafts posttransplant. In all groups, splenocyte pCTL frequencies were significantly lower than the corresponding values within the allograft. By comparison, no significant differences in intragraft or splenic proliferative T lymphocyte (pPTL) precursor frequencies were observed between any groups. These results indicate that unsensitized recipients of class I-disparate renal cells grafts are capable of maintaining graft survival in the early posttransplant period, despite the presence of significant in situ antidonor class I MHC-specific cellular immune responsiveness. These findings also indicate that long-surviving PVG recipients of class I-disparate renal allografts develop specific functional tolerance to donor class I alloantigens, that may be associated with a diminished frequency of anti-class I cytotoxic (but not proliferative) T cell precursors.

Animals↗

PubMed1994

[Influence of blood transfusion on cellular immunity after open heart surgery].

The effect of blood transfusion on cellular immunity was evaluated by measuring T cell subsets in 22 adult patients after open heart surgery. The patients were divided into two groups according to whether or not they received blood transfusions. There were no significant differences in pump time or aortic cross clamp time between the two groups. Leukocytosis was evident in both groups after open heart surgery, but the percentage to lymphocytes was reduced. The number of T cells were also reduced in both two groups. In the group that did not receive blood, the number of T cells were reduced the first day after surgery, but returned to preoperative levels two days later. Those that received blood transfusions had persistently low T cell counts three days after the operation. CD4 positive T cells were reduced the first day after operation but returned to preoperative levels three days after the operation in both groups. The percentage of CD8 positive T cells were unchanged in the group that didn't have a blood transfusion. CD8 positive T cells were significantly reduced three days post operatively in the group that received blood transfusions. The cellular immunity was disturbed for an extended period in the patients that received blood transfusions.

Adolescent↗

PubMed2005

Humoral and cellular immune responses to Fasciola gigantica experimental infection in buffaloes.

Humoral and cellular immune responses to Fasciola gigantica experimental infection in buffaloes were studied. The results showed that 33.4+/-9.1% of the infection dose was recovered as adult flukes from infected animals at necropsy. Significant differences of weight gain between infected and non-infected buffaloes was observed at 4 MPI (months post-infection). Anti F. gigantica excretory-secretory products (FgESP)-IgG levels increased significantly from 3 WPI (weeks post-infection) and displayed a peak at 13 WPI. Western blot indicated that in FgESP six major bands of 11.5, 19.0, 23.4, 29.8, 47.5 and 53.2kDa were recognized by F. gigantica-infected buffaloes sera after 0 WPI. Eosinophil numbers increased significantly from 3 WPI in F. gigantica-infected buffaloes and displayed a peak at 8 WPI. Peripheral blood mononuclear cells (PBMC) proliferation induced by FgESP increased from 2 WPI with a peak at 5 WPI. IFNgamma secretion by FgESP-stimulated PBMC appeared early from 1 WPI with three peaks at 2, 5 and 8 WPI, respectively. IL-10 production was observed from 2 WPI with two peaks at 4 and 9 WPI, respectively. Our results suggested that buffaloes were highly susceptible to F. gigantica infection, and this susceptibility could be associated with the late and weak cellular immune response in the early phase of infection and the Th0-like response throughout the infection.

Animals↗

PubMedDate not supplied

[Development of cellular immunity in experimental tick-borne encephalitis].

The development of cellular immunity was investigated in mice infected experimentally with tick-borne encephalitis virus strains (TBE) isolated from patients. In the presence of strain variants of the response, two main trends in the dynamics of cellular immunity induced by different virus strains were established: a rapid increase in the level of sensitization of lymphoid cells in the first days after virus inoculation followed in the stage of paralysis by the desensitization phenomenon (the dynamics of the waning type), and a gradual increase in the level of cellular response in the course of the infectious process (the dynamics of progressive type). The type of the dynamics and the level of immune response correlate with the clinical forms of TBE in man. A possible mechanism of the effect of the immunosuppressing properties of the virus on the immune response pattern in infected mice and the significance of the latter in TBE pathogenesis are discussed.

Animals↗

PubMed2001

Robust HIV type 2 cellular immune response measured by a modified anthrax toxin-based enzyme-linked immunospot assay.

Evaluation of immune mechanisms responsible for control of viral replication is critical to understanding HIV-2 attenuated biological characteristics in pathogenesis and transmission. Evaluation of the cellular immune response is often based on labor-intensive techniques that limit the scope of most studies performed. A simple and rapid anthrax toxin-based ELISPOT method to assess HIV-2 cellular immune response was developed. The modified anthrax toxin-based antigen presentation process performed better than a recombinant vaccinia system and the ELISPOT method significantly enhanced the ease and simplicity of the assay. Using this method, a robust HIV-2 cellular immune response directed toward the p26 core protein was exhibited in 21 of 24 (87.5%) infected women, and all 8 seronegative subjects were negative in both assays. Cellular immune responses were associated with low HIV-2 viral load. This simple and rapid modified anthrax toxin-based ELISPOT method allowed us to demonstrate, strong cellular immune responses that may be critical determinants in the HIV-2 attenuated phenotype.

Antigen Presentation↗

PubMed2003

A replication competent adenovirus 5 host range mutant-simian immunodeficiency virus (SIV) recombinant priming/subunit protein boosting vaccine regimen induces broad, persistent SIV-specific cellular immunity to dominant and subdominant epitopes in Mamu-A*01 rhesus macaques.

CTL are important in controlling HIV and SIV infection. To quantify cellular immune responses induced by immunization, CD8(+) T cells specific for the subdominant Env p15m and p54m epitopes and/or the dominant Gag p11C epitope were evaluated by tetramer staining in nine macaques immunized with an adenovirus (Ad) 5 host range mutant (Ad5hr)-SIVenv/rev recombinant and in four of nine which also received an Ad5hr-SIVgag recombinant. Two Ad5hr-SIV recombinant priming immunizations were followed by two boosts with gp120 protein or an envelope polypeptide representing the CD4 binding domain. Two mock-immunized macaques served as controls. IFN-gamma-secreting cells were also assessed by ELISPOT assay using p11C, p15m, and p54m peptide stimuli and overlapping pooled Gag and Env peptides. As shown by tetramer staining, Ad-recombinant priming elicited a high frequency of persistent CD8(+) T cells able to recognize p11C, p15m, and p54m epitopes. The presence of memory cells 38 wk postinitial immunization was confirmed by expansion of tetramer-positive CD8(+) T cells following in vitro stimulation. The SIV-specific CD8(+) T cells elicited were functional and secreted IFN-gamma in response to SIV peptide stimuli. Although the level and frequency of response of peripheral blood CD8(+) T cells to the subdominant Env epitopes were not as great as those to the dominant p11C epitope, elevated responses were observed when lymph node CD8(+) T cells were evaluated. Our data confirm the potency and persistence of functional cellular immune responses elicited by replication competent Ad-recombinant priming. The cellular immunity elicited is broad and extends to subdominant epitopes.

Adenoviruses, Human↗