Major histocompatibility complex restriction in tuberculosis susceptibility.
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Date
1997-01
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Abstract
More than one mechanism may contribute to disease susceptibility in tuberculosis,
viz., major histocompatability complex (MHC) restriction phenomenon, spectrum of immune
reactivity/cytokine profile and epidemiology induced anergy. Experiments from our laboratories
revealed that (i) human leucocyte antigen D-related allele 2 (HLA DR2) predispose for a more
severe form of pulmonary tuberculosis encoding a high responder status, (ii) spectrum of immune
reactivity to mycobacteria is 'innate', and it is demonstrable in healthy individuals from endemic
area, (iii) there is no correlation between the purified protein derivative (PPD) response and
peptide responses, (iv) once a person is high responder to P16 and P38 derived peptides (6/22),
he/she (whether a patient or control) is a high responder for a wide range of mycobacterial
peptides and (v)majority of the T-cell clones generated in vitro, to peptide 16ยท3 (amino acids
21-40) of 16 kA a mycobacterial antigen, in an HLA DR2 positive healthy individual is HLA DR
restricted, permissive and of Th1 phenotype. The results suggested that MHC class II restriction
play a role in peptide recognition and the immune response. Nonetheless the outcome and
specificity of the immune reactivity and the resultant disease pathogenesis may depend on the
promiscuity of peptide recognition and cytokine profiles.
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Keywords
MHC restriction, mycobacterial diseases, immune reactivity, responder status, peptides, cytokines
Citation
Pitchappan R M, Agrewala J N, Dheenadhayalan V, Ivanyi J. Major histocompatibility complex restriction in tuberculosis susceptibility. Journal of Biosciences. 1997 Jan; 22(1): 47-57.