RESUMO
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 16·3 (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.
RESUMO
The distribution of phenotypes of group specific component (Gc) was examined in 71 lepromatous leprosy (LL) patients without any history of ENL reaction and 65 LL patients with history of frequent episodes of ENL reaction. The distribution of none of the phenotypes of Gc (Gc 1-1, Gc 2-1, Gc 2-2) was statistically significant among these groups.