Leprosy is an infectious disease caused by non-cultivable bacteria Mycobacterium leprae.
Ridley and Jopling classified the disease into five polar forms, Tuberculoid (TT) and Lepromatous (LL),
in between two forms of the disease Borderline tuberculoid (BT), Borderline (BB) and Borderline
lepromatous (BL) are laid. The tuberculoid type (BT/TT) leprosy patients show good recall of cellmediated
immune (CMI) response and Th1 type of immune response, while lepromatous leprosy (LL)
patients show defect in cell-mediated immunity to the causative agent and Th2 type of immune response.
Due to distinct clinical and immunological spectra of the disease, leprosy attracted immunologists
to consider an ideal model for the study of deregulations of various immune reactions. Recent studies
show that Tregs, Th3 (TGF-β, IL-10), IL-35 producing Treg immune response associated with the
immune suppressive environment, survival of bugs. IL-17 producing Th17 immune response associated
with tuberculoid leprosy and play protective role. γδ T cells also increased from tuberculoid to lepromatous
pole of leprosy. In this review, we will discuss the role of various subtypes of T-cell and their cytokines
in the pathogenesis of leprosy.