Analysis of T-cell and B-cell responses to recombinant M. leprae antigens in leprosy patients and in healthy contacts: significant T-cell responses to antigens in M. leprae nonresponders.

The recognition of a panel of recombinant Mycobacterium leprae antigens by T cells and B cells from 29 borderline tuberculoid/tuberculoid (BT/TT) and 18 lepromatous leprosy (LL) patients and from 21 healthy controls (HC) in leprosy-endemic regions of Ethiopia was examined. All 11 antigenic molecules tested (including M. leprae hsp 10, hsp18, hsp65 and several novel M. leprae antigens) were shown to be recognized by T cells, but clear quantitative differences existed between reactivities induced by individual antigens. Similar quantitative differences were observed when antibody responses to hsp10 and hsp65 antigens were determined. No associations were found between the antigen-specific responses and the subject status of either BT/TT and LL patients or HC. Fifteen percent of the patients who were nonresponsive to sonicates of M. leprae showed significant T-cell responses to one or more individual M. leprae antigens. This indicates that M. leprae constituents other than the proteins tested are responsible for the M. leprae-specific nonresponsiveness in these patients, which may be exploited for the design of vaccines or immunotherapeutic modalities aimed at inducing M. leprae-specific immunity in nonresponders.

Thalidomide does not perturb CD2, CD4, CD5, CD8, HLA-DR, or HLA-A, B, C molecules in vitro on the membranes of cells with immune potential.

Thalidomide dramatically relieves the signs and symptoms of erythema nodosum leprosum (ENL). ENL is an acute inflammatory complication of lepromatous leprosy. The cause(s) of ENL as well as the mechanism of action of thalidomide in arresting ENL are unknowns. It has been suggested that ENL is the consequence of a transient activation of a cell-mediated-immune (CMI) response to Mycobacterium leprae. To initiate a CMI response, an interaction between adhesion and/or signal transducing molecules on T-cells and molecules on antigen presenting cells would occur. An alteration, induced by thalidomide, of one or more of the molecules on T-cells or antigen presenting cells that are essential to maintaining the reactive state of ENL, could explain Thalidomide's ability to attenuate ENL. Thalidomide did not modify: (a) adhesion and/or signal transducing molecules such as CD2, CD4, CD5 and CD8, or (b) molecules that facilitate antigen presentation such as HLA-DR, HLA-A, HLA-B, or HLA-C.