Affiliation:
1. Department of Pharmacology Institute of Postgraduate Medical Education and Research Kolkata India
2. Multidisciplinary Research Unit (MRU) Institute of Postgraduate Medical Education and Research Kolkata India
3. Department of Microbiology Sarat Chandra Chattopadhyay Govt. Medical College and Hospital, Uluberia Howrah India
4. Department of Tropical Medicine School of Tropical Medicine Kolkata India
Abstract
ABSTRACTIn visceral leishmaniasis, the Type II helper T cell predominance results in B cell modulation and enhancement of anti‐leishmanial IgG. However, information regarding its dermal sequel, post‐kala‐azar dermal leishmaniasis (PKDL), remains limited. Accordingly, this study aimed to elucidate the B cell‐mediated antibody‐dependent/independent immune profiles of PKDL patients. In the peripheral blood of PKDL patients, immunophenotyping of B cell subsets was performed by flow cytometry and by immunohistochemistry at lesional sites. The functionality of B cells was assessed in terms of skin IgG by immunofluorescence, while the circulating levels of B cell chemoattractants (CCL20, CXCL13, CCL17, CCL22, CCL19, CCL27, CXCL9, CXCL10 and CXCL11) were evaluated by a multiplex assay. In patients with PKDL as compared with healthy controls, there was a significant decrease in pan CD19+ B cells. However, within the CD19+ B cell population, there was a significantly raised proportion of switched memory B cells (CD19+IgD−CD27+) and plasma cells (CD19+IgD−CD38+CD27+). This was corroborated at lesional sites where a higher expression of CD20+ B cells and CD138+ plasma cells was evident; they were Ki67 negative and demonstrated a raised IgG. The circulating levels of B cell chemoattractants were raised and correlated positively with lesional CD20+ B cells. The increased levels of B cell homing markers possibly accounted for their enhanced presence at the lesional sites. There was a high proportion of plasma cells, which accounted for the increased presence of IgG that possibly facilitated parasite persistence and disease progression.
Funder
Indian Council of Medical Research
Department of Health Research, India