Vivax infection alters peripheral B‐cell profile and induces persistent serum IgM. (11th September 2018)

• Record Type: Journal Article
• Authors: Patgaonkar, Mandar; Herbert, Fabien; Powale, Krushali; Gandhe, Prajakta; Gogtay, Nithya; Thatte, Urmila; Pied, Sylviane; Sharma, Shobhona; Pathak, Sulabha
• Is Part Of: Parasite immunology. Volume 40:Number 10(2018)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2018-09-11
• Subjects: atypical memory B cells -- autoreactivity -- B‐cell development -- dengue -- IgM repertoire -- immature B cells -- PANAMA blot -- vivax malaria; Veterinary parasitology -- Immunological aspects -- Periodicals; Host-parasite relationships -- Immunological aspects -- Periodicals; 571.96
• DOI: 10.1111/pim.12580
• Languages: English
• ISSNs: 0141-9838

Abstract

Summary: B cell–mediated humoral responses are essential for controlling malarial infection. Studies have addressed the effects of Plasmodium falciparum infection on peripheral B‐cell subsets but not much is known for P. vivax infection. Furthermore, majority of the studies investigate changes during acute infection, but not after parasite clearance. In this prospective study, we analysed peripheral B‐cell profiles and antibody responses during acute P. vivax infection and upon recovery (30 days post‐treatment) in a low‐transmission area in India. Dengue patients were included as febrile‐condition controls. Both dengue and malaria patients showed a transient increase in atypical memory B cells during acute infection. However, transient B cell‐activating factor (BAFF)–independent increase in the percentage of total and activated immature B cells was observed in malaria patients. Naïve B cells from malaria patients also showed increased TLR4 expression. Total IgM levels remained unchanged during acute infection but increased significantly at recovery. Serum antibody profiling showed a parasite‐specific IgM response that persisted at recovery. A persistent IgM autoantibody response was also observed in malaria but not dengue patients. Our data suggest that in hypoendemic regions acute P. vivax infection skews peripheral B‐cell subsets and results in a persistent parasite‐specific and autoreactive IgM response.