Molecular typing of HLA class I and class II antigens in Indian kala-azar patients
ABSTRACT HLA has been shown to be associated with many diseases. To find out whether host genetic factors like the HLA are involved in susceptibility to kala-azar (visceral leishmaniasis) in India, we formulated an association study with genetically related controls. All samples were typed by PCR SSOP (sequence specific oligonucleotide probes) for HLA class I (A and B) and class II (DR) antigens. The test of association we used was the transmission disequilibrium test (TDT). No significant evidence for association with any of the three HLA loci was obtained.
- SourceAvailable from: panacea-biotec.com[Show abstract] [Hide abstract]
ABSTRACT: 1-4 Most studies have found the primary non response rate to recombinant hepatitis B vaccination to range between 5% and 10%. Factors that have been linked to non-response include age, sex, obesity, smoking, diabetes and chronic renal failure. 1,4,5-7 But these factors alone cannot explain all causes of non-response. It has The average age of the responders was 44.6 ± 6.9 years. The male-to-female ratio in the responder population was 4:1 while in the non-responder population it was 8:7. Table 1 shows the frequency of specific HLA types among responders and non-responders. Haplotypes with the highest frequencies among non responders (compared to responders) were HLA A1 and B15 (5-times) following by B40 (3 times), and A10 and DQ2 (2.5 times). DR 52 was present in a frequency of 11/15 (73.3%) in equal measure in both groups. HLA A1 and B15 were present among 5/15 of the non-responders (33.3%) but only 1/15 of the responder population (6.7%). HLA DR53 was more frequent in the non- responders (7/15, 46.7%) compared to the responders (5/15, 33.3%). The most common HLA phenotypes in the responder population were HLA - A11, C3, DR10 and DR51. These differences in frequencies were however non-significant (p>0.05).
- [Show abstract] [Hide abstract]
ABSTRACT: The human impact of visceral leishmaniasis is significant. Some 500,000 new cases are reported annually, and epidemics may decimate local populations. A more complete understanding of the human immune response and its pathological consequences are needed for the design of vaccines and for improvements in therapy. This will require more thorough clinical investigation, and also a better appreciation of the usefulness and limitations of animal models. This review will concentrate on recent observations on patients with active VL. It will summarize recent progress in studies using a murine model that may have most bearing on human disease. Finally, it discusses future research directions aimed at elucidating the pathogenesis of VL.
- [Show abstract] [Hide abstract]
ABSTRACT: Human leukocyte antigens (HLAs) are an inherent system of alloantigens, which are the products of genes of the major histocompatibility complex (MHC). These genes span a region of approximately 4 centimorgans on the short arm of human chromosome 6 at band p 21.3 and encode the HLA class I and class II antigens, which play a central role in cell-to-cell interaction in the immune system. These antigens interact with the antigen-specific cell surface receptors of T lymphocytes (TCR) thus causing activation of the lymphocytes and the resulting immune response. Class I antigens restrict cytotoxic T-cell (CD8+) function thus killing viral infected targets, while class II antigens are involved in presentation of exogenous antigens to T-helper cells (CD4+) by antigen presenting cells (APC). The APC processes the antigens, and the immunogenic peptide is then presented at the cell surface along with the MHC molecule for recognition by the TCR. Since the MHC molecules play a central role in regulating the immune response, they may have an important role in controlling resistance and susceptibility to diseases. In this review we have highlighted studies conducted to look for an association between HLA and infectious diseases; such studies have had a variable degree of success because the pathogenesis of different diseases varies widely, and most diseases have a polygenic etiology.Emerging infectious diseases 01/1997; 3(1):41-9. DOI:10.3201/eid0301.970105 · 7.33 Impact Factor