Chronic infection with trypanosoma cruzi alters the phenotypic profile of circulating memory B cells in humans (MPF2P.812)

Trypanosoma cruzi was shown to induce the loss of parasite-specific IgG-producing B cells during the acute infection of mice, which was proposed to hamper B cell responses and favor parasite replication and chronicity (Zuniga et al. 2002). Herein, we measured the levels of circulating memory and MZ-like B cells in 12 individuals chronically infected with T. cruzi and 9 healthy controls based on the expression of CD19, IgM IgD, IgG, and CD27. T. cruzi-infected individuals had significantly lower percentages of IgM+IgD-CD27+ (IgM-only), IgM-IgD-CD27+ (isotype-switched) and IgG+IgD-CD27+ memory B cells compared to controls (p<0.05). Also, the percentage of IgM+IgD+CD27+ (MZ-like) B cells was reduced in infected individuals while the proportion of IgG+IgD-CD27- memory B cells was increased (p<0.05). The levels of memory B cells were further analyzed according to ECG findings in infected individuals (asymptomatic [ASY] and chronic Chagas heart disease [CHD]). IgG+IgD-CD27+, IgM+IgD-CD27+ and IgM-IgD-CD27+ B cells were significantly reduced in the ASY group compared to controls (p<0.05); CHD individuals had decreased levels of IgM-IgD-CD27+ and IgM+IgD-CD27+ B cells (p<0.05). Altogether, our data indicate that chronic exposure to T. cruzi modulates the phenotypic profile of the peripheral blood CD19+ B cell compartment in humans, and that some of the defects develop early in the infection, prior the onset of heart symptoms. Supported by Argentinian MINCYT/FONCYT PICT 2010-2148