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At least 649 records · Page 36Linked to original sources
PubMed1990

Leishmania major: nature of immunity induced by immunization with a mutagenized avirulent clone of the parasite in mice.

A chemically mutagenized avirulent form of Leishmania major was used to immunize BALB/c and C57B1/6 mice against challenge with virulent L. major. Immunity was elicited when the avirulent parasite was injected intravenously or intraperitoneally, but not subcutaneously. In fact, the latter route of immunization sometimes resulted in exacerbation of a subsequent infection with virulent L. major. Mice immunized with avirulent L. major developed upon challenge with virulent L. major cutaneous lesions which were significantly smaller and contained substantially fewer parasites than lesions on control nonimmune animals. Finally, the protection conferred by immunization with avirulent L. major could be adoptively transferred with T cells of the CD4+ lineage but not the CD8+ lineage.

Animals↗
PubMed1987

Nature of immune complexes in autoimmune chronic active hepatitis.

Immune complexes containing antinuclear antibodies have been observed in autoimmune chronic active hepatitis. Using a library of nuclear constituents (deoxyribonucleic acid, small nuclear ribonucleoproteins, and histones), we analyzed the antigens involved in formation of immune complexes. Immune complexes were defined in dissociation experiments, and after separation under dissociating conditions. Immune complexes composed of histones and immunoglobulin G were observed in four of nine immune complex-positive autoimmune chronic active hepatitis sera. Immune complexes containing the small nuclear ribonucleoprotein U1-RNP and immunoglobulin G were observed in two additional samples. Kidney eluates obtained from 2 patients with autoimmune chronic active hepatitis and membranous glomerulonephritis revealed enrichment of anti-U1-RNP, suggesting specific deposition of this antibody in complexed form. Circulating immune complexes containing histones were observed only in patients with autoimmune chronic active hepatitis-associated sicca syndrome; those containing U1-RNP were restricted to patients with autoimmune chronic active hepatitis associated with kidney disease.

Antibodies, Antinuclear↗
PubMed1985

The nature of immunity to Snyder-Theilen fibrosarcoma virus induced tumors in cats.

Snyder-Theilen fibrosarcoma virus (ST-FeSV) induced tumors evoked a vigorous immune response in adolescent cats. The response was characterized histologically by a lymphoid and histiocytic cell infiltrate beginning around the 9th day post inoculation. Hyperemia edema, hemorrhage, and necrosis of the tumors occurred shortly thereafter. Gross regression of the tumors commenced around the 15th day. Viable fibrosarcoma cells could be recovered as almost pure cultures from tumors biopsied on the 9th day. Biopsies taken between days 9 and 15 contained progressively fewer tumor cells and increasing numbers of lymphoid cells, histiocytes, giant cells, and normal fibroblasts. Tumor cells in such mixed cultures did not replicate as fast as normal and died out within 7 to 14 days. Viable tumor cells were not recovered from biopsies taken after day 15. Fibrosarcoma regression was associated with the appearance of tumor cell specific cytotoxic lymphocytes and antibodies in the blood. Cell mediated immunity, as determined by a chromium release assay, consisted of both antibody dependent and independent mechanisms. Fluorescent and complement dependent cytolytic antibodies were detected in the blood at the same time as cytotoxic lymphocytes, but persisted after regression. In a preliminary experiment, serum from tumor regressor cats was injected into susceptible kittens, and the kittens were then challenged with ST-FeSV transformed fibroblasts or whole FeSV. Immune serum did not prevent the appearance of initial growth of tumors, but did slow their subsequent growth and increased the rate of regression. Immune serum had a much more dramatic inhibitory effect on the accompanying retrovirus infection.

Animals↗
PubMed1993

Does HIV disrupt a naturally occurring immune modulation system?

An immune modulation complex is proposed which recognizes and is driven by an MHC presented epitope of the CD4 molecule present on the surface of up regulated CD4+ lymphocytes. Immune modulation is affected by both CD4 lymphocyte destruction and impairment of their potential for immune recognition. These two processes are carefully controlled by an idiotypic, anti-idiotypic feedback mechanism. The CD4 tropic area of HIV impersonates some components of that feedback loop resulting in increased CD4 lymphocyte destruction.

Animals↗
PubMed1978

Phylogenetic origins of immune recognition: naturally occurring DNP-binding molecules in chordate sera and hemolymph.

A method is described which allows the isolation of small quantities of DNP-binding antibodies of both high- and low-molecular-weight classes. The only detectable DNP-binding protein in the serum of placoderm-derived vertebrates was immunoglobulin in nature, and of the order of less than or equal to 1% total serum immunoglobulin. Proteins in the serum of the urochordate Pyura stolonifera, which bind to both DNP and erythrocyte antigens, showed charge heterogeneity and an apparent subunit molecular weight of approximately 65,000 to 70,000 daltons.

Animals↗
PubMed1991

Naturally acquired immunity to Plasmodium falciparum.

Malaria infections induce multiple humoral and cellular responses, most of which are probably not protective. This discussion of the epidemiology of acquired immunity to malaria will concentrate on two main areas: first, the relationship between parasitism and disease in endemic settings and the constraints placed on determining which responses are important in acquired protective immunity; second, the central importance of antigenic diversity in the host-parasite relationship. The emphasis throughout, unless otherwise stated, will be on the major human pathogen Plasmodium falciparum.

Animals↗
PubMed1998

Natural human immunity to trypanosomes.

Complement-dependent destruction of invading micro-organisms is a crucial first-line defense against infection, yet both African and American trypanosomes are able to resist attack by complement. African trypanosomes resist non-specific complement attack by virtue of a thick glycoprotein surface coat, and the host range of certain African trypanosomes is believed to be defined by their susceptibility to a subclass of human high density lipoprotein (HDL) and/or a high molecular weight protein complex present in human serum. In the first part of this review, Stephen Tomlinson and Jayne Raper look at the properties and mechanisms of action of these trypanolytic factors on African trypanosomes, and discuss briefly the possible mechanisms whereby these human pathogens resist lysis by human serum. The mechanisms that enable the American trypanosome Trypanosoma cruzi to resist complement attack are reviewed in the second part of this article.

Journal Article↗