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PubMedDate not supplied

Immunopathology of American cutaneous leishmaniasis. Modulation of MHC class II gene products by keratinocytes before and after glucantime therapy.

Epidermal changes from 32 cutaneous and 3 mucosal American cutaneous leishmaniasis (ACL) active lesions were studied for HLA-DR, -DQ and -DP expression, Langerhans cells and lymphocyte infiltration. In addition to a DR and DQ positivity at the surface of the cells of the inflammatory infiltrate, a strong reaction for DR antigens was detected on keratinocytes. Hyperplasia of Langerhans cells was present in all cutaneous lesions and epidermis was infiltrated by T lymphocytes. When healed lesions of 14 of these subjects were re-biopsied 1 to 12 months after the end of pentavalent antimonial therapy, MHC class II antigens could no longer be seen on keratinocytes. Our data represent evidence for the reversibility of the abnormal HLA-DR expression by keratinocytes in ACL after Glucantime therapy or spontaneous scar formation, demonstrating that this expression is restricted to the period of active lesions. The present findings can be regarded as an indirect evidence that keratinocytes may be involved in the immunopathology of ACL.

Antiprotozoal Agents↗
PubMedDate not supplied

Functional expression of a transfected murine class II MHC gene.

The activation of T helper lymphocytes involves the recognition of class II major histocompatibility complex antigens, which are dimeric glycoproteins (of subunit composition A alpha A beta or E alpha E beta) expressed on the surfaces of macrophages and B lymphocytes. One approach to understanding the relationship between the structure of these antigens and their functions in the immune response is to clone the genes that encode them, to obtain functional expression of the cloned genes transfected into an appropriate cell line, and then to see how those functions are affected in variant genes generated in vitro. We report here the expression in Iad-bearing B cells of an Ak beta gene, which confers on the transfected cells the capacity for both allostimulation and antigen-dependent activation of an I-Ak-restricted T-cell clone.

Animals↗
PubMed1994

Ectopic expression of gamma interferon in the eyes of transgenic mice induces ocular pathology and MHC class II gene expression.

PURPOSE: To direct the expression of gamma IFN to the eyes of transgenic mice as a means of investigating the possible role of this lymphokine in ocular pathogenesis. METHODS: Transgenic mouse strains were generated by injection of a DNA fragment containing the murine alpha A-crystallin promoter fused to the coding sequence of murine gamma IFN gene. PCR and RT-PCR were used to screen for the presence of the transgene and mRNA analyses, respectively. Methacrylate-embedded eye sections were analyzed for morphology and cryosections for immunoperoxidase antibody staining. RESULTS: The most notable effects of gamma IFN in these transgenic mice include cataract, microphthalmia, blepharophimosis, microphakia, impairment of lens fiber formation, arrest of retinal differentiation, serous retinal detachment with presence of macrophages in the subretinal space, persistent hyperplastic primary vitreous, and corneal vascularization. MHC class II mRNA levels were significantly increased in the transgenic eyes and MHC class II proteins were expressed in their cornea, iris, ciliary body, choroid, lens and RPE. CONCLUSIONS: Ectopic expression of gamma IFN in the lens affected the growth of the whole eye, resulting in microphthalmia and microphakia. The author's data suggest that alpha ACry-gamma IFN transgenic mouse ocular cells express functional gamma IFN receptors and that interaction of gamma IFN with its receptor induced biochemical and morphologic changes in the transgenic eyes. These mice provide an animal model for the study of the linkage between aberrant MHC expression and predisposition to autoimmune diseases.

Animals↗
PubMed1992

The genes for MHC class II regulatory factors RFX1 and RFX2 are located on the short arm of chromosome 19.

RFX1 is a transacting DNA-binding regulatory factor involved in the control of MHC class II gene expression. RFX2 is a structurally very similar protein with identical DNA binding features. A member of the family of RFX factors is affected in an autosomal recessive disease, MHC class II deficient combined immunodeficiency (CID), caused by a defect in a trans-acting regulatory factor controlling MHC class II gene expression. In situ hybridization with 3H-labeled RFX1 cDNA has allowed us to identify two distinct targets on the short arm of chromosome 19 (19p13.1 and 19p13.2-p13.3). With the use of biotinylated genomic cosmid clones specific for RFX1 and RFX2, respectively, it was then possible to localize RFX1 at 19p13.1 and RFX2 at 19p13.2-p13.3. These two regulatory genes are thus assigned to a region of high gene density and RFX1 is close to another DNA-binding factor, LYL1.

Chromosome Mapping↗
PubMed1988

Positive selection of CD4+ thymocytes controlled by MHC class II gene products.

The mature T-cell antigen receptor repertoire is characterized by lack of reactivity to self-components as well as by preferential reactivity to foreign antigens in the context of polymorphic self-proteins encoded within the major histocompatibility complex. Whereas the former characteristic (referred to as negative selection or tolerance) is associated with intrathymic deletion of T cells expressing T-cell antigen receptor beta-chain variable (V beta) domains, which confer a preferential reactivity to self antigens, the existence of the latter (referred to as positive selection or MHC restriction) has so far only been inferred indirectly from functional studies. We show here that intrathymic deletion of V+beta 6 T cells (reactive with a self-antigen encoded by the Mlsa locus) is controlled by polymorphic MHC class II determinants. Furthermore, in mice lacking expression of Mlsa, the same class II MHC loci control the frequency of occurrence of V+beta 6 cells among mature CD4+ T lymphocytes. These data are direct evidence for positive selection by MHC determinants in the thymus in unmanipulated animals.

Animals↗
PubMed1986

The mouse E beta 2 gene: a class II MHC beta gene with limited intraspecies polymorphism and an unusual pattern of transcription.

Analysis of genomic clones containing the E beta 2 region from the mouse major histocompatibility complex (MHC) reveals a gene that is similar to conventional class II beta genes in its overall organization and sequence but unusual in that it shows limited intraspecies allelic polymorphism. Like the conventional class II beta genes, the E beta 2 gene is transcriptionally active in a variety of B lymphoid cells. However, its transcripts consist of multiple polyadenylated species from 1.8 to 3.6 kb in size which are present at only approximately 1/20 the level of E beta 1 mRNA in the same cells. In addition, unlike other class II genes, E beta 2 transcription is not induced by gamma-interferon treatment of macrophage/monocyte tumor lines. These distinctive features suggest that the E beta 2 gene product may have a unique functional role, different from that of previously studied class II proteins.

Amino Acid Sequence↗
PubMedDate not supplied

Loss of polymorphic restriction fragments of class I and class II MHC genes in a malignant melanoma.

DNAs from human malignant melanoma cells and autologous peripheral blood lymphocytes were evaluated by Southern blot analysis with probes for class I and II HLA genes. DNA of melanoma cells digested with PvuII, EcoRI and BglI and hybridized with a DR beta probe showed a loss of several fragments when compared with DNA from lymphocytes. The same DNAs were not distinguishable when hybridized with a DQ beta probe. Analysis of melanoma and autologous lymphocyte DNAs from the same patient with a class I cDNA, after digestion with several endonucleases, revealed a further loss of fragments in melanoma cells. Comparison of restriction fragment patterns of melanoma and lymphocytes with those of homozygous, serologically-typed cell lines indicated that melanoma cells have lost fragments diagnostic of DR2 and A1 antigens. A densitometric analysis of signals of several oncogenes in comparison with that of DR indicated that a duplication of the remaining DR allele had occurred in melanoma cells.

DNA, Neoplasm↗
PubMed1988

Restriction fragment length polymorphisms of horse class II MHC genes observed using various human alpha- and beta-chain cDNA probes.

Genomic DNA isolated from 20 horses was digested with up to six restriction endonucleases and subjected to southern blot hybridization analysis using various human class II alpha- and beta-chain cDNA probes. A high degree of restriction fragment length polymorphism (RFLP) was found for the DQ alpha, DP beta, DQ beta and DR beta probes, about 20 polymorphic bands being detected for each. DR alpha showed 2-4 polymorphic bands, whereas no evidence for DP alpha-like genes was found. A number of correlations of RFLPs with individual alloantisera were apparent.

Animals↗
PubMed1990

Class I and class II MHC gene products differentially affect the fate of V beta 5 bearing thymocytes.

We have previously shown that T cells bearing V beta 5+ T-cell receptors (TCRs) are frequent in B10 (H-2b) and B10.Q (H-2q) mouse strains but are rare in the congenic strain B10.BR (H-2k). Furthermore, we have found that V beta 5 bearing T cells appear to be excluded from the B10 alloresponse to I-Abm12 despite the participation of most other V beta bearing cells. To further study MHC effects on V beta 5 expression, we have generated two V beta 5 specific monoclonal antibodies and show here that V beta 5 expressing T cells are clonally deleted from strains expressing a class II, I-E molecule. Furthermore, I-E- strains generate few CD4+ V beta 5+ T cells despite significant numbers of V beta 5+ T cells in the CD8+ subset. Thus, V beta 5 bearing T cells are positively selected by class I MHC molecules, clonally deleted by class II I-E molecules, and poorly selected by class II I-A molecules.

Amino Acid Sequence↗
PubMed1989

Evidence that IFN-gamma does not affect MHC class II gene expression at the post-transcriptional level in a mouse macrophage cell line.

Mouse class II major histocompatibility complex genes have been shown to be regulated at the level of transcription for both tissue-specific and inducible expression. In particular, IFN-gamma induction of the class II genes has been shown to occur at the transcriptional level, although the role that additional post-transcriptional mechanisms of regulation may play in this induction is not known. To evaluate IFN-gamma effects on transcriptional and post-transcriptional events of class II gene expression, we examined the rate of decline of class II transcription, steady-state mRNA, and cell surface protein following the removal of IFN-gamma from maximally stimulated WEHI-3 cells (an IFN-gamma inducible, myelomonocytic cell line). We determined that transcription of class II genes almost completely returned to baseline levels eight hours after removal of IFN-gamma. However, the steady-state level of class II mRNA's required 4 days, and membrane Ia expression required 5 days to return to baseline levels. This decay was linear and allowed us to determine a half-life value of 16-20 h for class II transcripts. These data demonstrate that, following removal of IFN-gamma from fully stimulated cells, transcription of the class II genes declined rapidly, but mRNA was quite long-lived. We also assessed the class II mRNA stability in unstimulated WEHI-3 cells and the B-cell lymphoma. A20/2J, by actinomycin D treatment and northern blot analysis. In agreement with the IFN-gamma washout experiments, transcripts from all four class II genes were quite long-lived in these cell types, with a half-life greater than ten hours. These data support the concept that IFN-gamma acts primarily at the level of class II transcription and argues against IFN-gamma playing a major role in post-transcriptional modulation of class II expression.

Animals↗