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At least 199 records · Page 11Linked to original sources

Cellular immune responses are essential for the development of Helicobacter felis-associated gastric pathology.

The bacteria Helicobacter pylori is a major human pathogen that infects over half of the world's population. Infection initiates a series of changes in the gastric mucosa, beginning with atrophic gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and gastric adenocarcinoma. Although this cascade of events clearly occurs, little is known about the role of the host immune response in disease progression. We have utilized the C57BL/6 Helicobacter felis mouse model to critically analyze the role of the adaptive immune response in the development of Helicobacter-associated gastric pathology. Infection of B and T cell-deficient RAG-1-/- mice or T cell-deficient TCRbetadelta-/- mice with H. felis resulted in high levels of colonization, but no detectable gastric pathology. Conversely, infection of B cell-deficient microMT mice resulted in severe gastric alterations identical with those seen in immunocompetent C57BL/6-infected mice, including gastric mucosal hyperplasia and intestinal metaplasia. These results demonstrate that the host T cell response is a critical mediator of Helicobacter-associated gastric pathology, and that B cells and their secreted Abs are not the effectors of the immune-mediated gastric pathology seen after H. felis infection. These results indicate that in addition to specific Helicobacter virulence factors, the host immune response is an important determinant of Helicobacter-associated disease.

Animals↗

[An evaluation of the effect of 2,4-dichlorophenoxyacetic acid derivatives on humoral and cellular immunities].

A single oral administration of phenoxy herbicides, viz. 2,4-dichlorophenoxyacetic acid (2,4-D), amino salt, sodium salt, diethylene glycol, iso-octyl and octyl ethers in a dose of LD16, was found to produce a pronounced suppressive effect on humoral immunity on day 5. The 2,4-D derivatives under study, administered in the same dose, stimulated the manifestations of delayed-type hypersensitivity in mice immunized with sheep red blood cells. The effect of the inhibition of antibody formation to thymus-dependent antigen ranged in the order of the increase in the toxicity of substances: amino salt, diethylene glycol ether, 2,4-D, sodium salt, iso-octyl and octyl ethers. On the contrary, the intensity of delayed-type hypersensitivity was more pronounced with regard to substances having greater toxicity.

2,4-Dichlorophenoxyacetic Acid↗

Humoral and cellular immune responses to the GB virus C/hepatitis G virus envelope 2 protein.

Immune responses to two recombinant envelope 2 (E2) proteins, representing genotypes 1 and 2 of the GB virus C, or the hepatitis G virus (GBV-C/HGV), were studied in mice and in 48 individuals with, or without, chronic, or past GBV-C/HGV infection. Immunised mice developed E2-specific antibodies (mean titres, 1:1,167 to 1:9,360), recognising linear antigenic regions and proliferative and IL-2, IL-6 and gammaIFN cytokine responses regardless of the viral genotype. Individuals with past GBV-C infection had E2 antibody titres from 1:1,500 to 1:7,500 that did not recognise the E. coli derived E2 protein or linear antigenic regions. Proliferative E2-specific responses were detected in peripheral blood mononuclear cells from 6/22 (27%) persons with, and in none without GBV-C markers (P<0.05). Thus, E2-specific immune responses are mainly crossreactive between different variants of GBV-C/HGV, although proliferative responses appear to be rare.

Amino Acid Sequence↗

Naturally formed or artificially reconstituted non-covalent alpha2-macroglobulin-peptide complexes elicit CD91-dependent cellular immunity.

Immunization of mice with in vitro reconstituted alpha2-macroglobulin-peptide complexes primes peptide-specific CTL responses. We show here using the H-Y antigenic system that naturally produced, immunogenic alpha2-macroglobulin-peptide complexes can be isolated from the sera of normal male mice. As an application of these ideas to cancer immunity, we show that the immunity evoked by alpha2-macroglobulin-peptide complexes reconstituted in vitro is effective in prophylaxis against tumors. Furthermore, complex peptide mixtures isolated from tumor lysates can be reconstituted non-covalently with alpha2-macroglobulin and such complexes elicit potent protective tumor immunity. This approach circumvents the need for prior knowledge of the identity of the immunogenic peptides. The heat shock protein/alpha2-macroglobulin receptor CD91 is shown to be involved in the ability of heat shock proteins or alpha2-macroglobulin to elicit an anti-tumor immune response.

Animals↗

[Cellular immunity indices in combined chronic exposure to stress and low concentrations of carbon monoxide (II). Experimental research].

Studies of the chronic combined effects of carbon monoxide low concentrations and psychoemotional stress revealed changes in the peripheral lymphocyte subpopulation in all groups of examinees, connected with the defense activation of the humoral immunity and functional decrease of T lymphocytes. Analysis of correlations of cell subpopulations revealed disorders of their relationships, augmenting with the intensity of exposure. Combined action of carbon monoxide in the maximal of studies concentrations with stress resulted in the most severe changes of nonspecific immunity, which proves decompensated decrease of immunity.

Animals↗

[Mechanism of cellular immunity accommodation in prophylactic effects of nasal tolerance with dual analogue on experimental autoimmune myasthenia gravis in Lewis rats].

OBJECTIVE: To study the mechanism of prophylactic effects of nasal tolerance with a dual analogue (Lys262-Ala207) on experimental autoimmune myasthenia gravis (EAMG). METHODS: Clinical and immunological changes were observed in Lewis rats administered with dual analogue Lys262-Ala207 nasally, to compare the effects between the rats with predetermined dosage of Lys262-Ala207 and control peptides at two different time points, before the day (Group A or C) or on the day (Group B or D) of immunization with acetylcholine receptor (AChR) in complete Freud's adjuvant for 10 consecutive days. The clinical scores was evaluated for 50 days post immunization. Numbers of MNC expressing IFN-gamma, IL-4 or IL-10 and CD4+ and/or CD25+ from lymph nodes were enumerated by flow cytometry. Proliferative response, expressed as stimulation index (SI), was suppressed in response to antigen-specific stimulation in the rats receiving dual analogue, as compared with the rats receiving saline buffer only. RESULTS: Group A and group B of Lewis rats developed EAMG with reduced severity, as compared to the control groups. Number of cells synthesizing IFN-gamma, IL-4 or IL-10 decreased, whereas numbers of CD4+CD25+ cells increased in group A and B than those in the control groups. Proliferative response was suppressed in response to antigen-specific stimulations in the rats receiving dual analogue Lys262-Ala207. CONCLUSIONS: Nasal administration with a dual analogue Lys262-Ala207 at two different time points, before the day and on the day of immunization, could delay symptoms of muscular weakness in EAMG rats, which was associated with suppression of immune function in AChR antigen-specific T cells and lay a scientific foundation for treatment of human MG with nasal dual analogue.

Administration, Intranasal↗

[The cellular immunity indices of patients with a rheumatic heart defect].

In 29 patients with clinical diagnosis of rheumatic valvular disease the quantitative values of active rosettes and the specific sensitization to human heart myosin were examined. The specific sensitization to human heart myosin was examined by two methods concurrently: method of inhibiting leucocyte migration in agarose and method for direct specific lymphocytolysis with myosin. The results were compared with those of 44 clinically healthy controls. In the patients with rheumatic valvular disease (RVD) the values of the active rosettes are significantly lower (p less than 0.01) than in the healthy controls. With the method of direct specific lymphocytolysis with myosin statistically significant sensibilization of the lymphocytes to myosin was found in the patients with RVD (p less than 0.001). In 5 patients examined before and after operation it was established that 2-4 weeks after a successful correction of the hemodynamics the specific sensibilization of the lymphocytes to myosin was no more present.

B-Lymphocytes↗

[The effect of biocarbazine on the indices of humoral and cellular immunity in mice].

Biocarbazin (5-3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide) when administered in different doses and schedules depressed the primary immune response of mice to erythrocytes (SE). A dose-dependent effect on the immunosuppression degree is revealed. Both the inductive and productive stages of antibody formation are sensitive to the immunosuppressive action of the agent. Under certain conditions biocarbazin induced a sharp suppression of humoral immune response. At the same time, it enhanced significantly the delayed-type hypersensitivity (DTH) response to SE.

Animals↗

[Development of a cellular immune response in a highly cancer-susceptible C3H/He strain of mice and its nonfactor substrain C3H/f after the transplantation of a syngeneic mammary gland tumor].

Syngeneic mammary gland tumor (MMT-1) grew slower in non-factor C3H/f (MTV-L) mice than in wirus-positive C3H/He (MTV-S) mice. The immunization of mice with tumor (MMT-1), inoculated and later excised, revealed a higher immune reactivity in the mice of the non-factor substrain. In studying the dynamics of the cytotoxic activity of lymphocytes in regional lymph nodes cytotoxically active lymphocytes were found to appear in C3H/f mice on day 6 after the inoculation of tumor (MMT-1), while the areactive state of lymphocytes was observed in C3H/He mice on days 3 and 24 and in C3H/f mice on day 24 after the inoculation of tumor (MMT-1). Spleen lymphocytes in C3H/f mice had no cytotoxic effect on tumor cells.

Animals↗