Abstract
Experimental leishmaniasis is widely used to study the effector functions of T helper cell subsets in vivo. Healing and nonhealing Leishmania major infections have been correlated with T helper 1 and T helper 2 responses, respectively. In the present study, we determined T cell effector functions ex vivo, without any further restimulation and compared them to those obtained following antigen-specific restimulation in vitro. Our results show that T helper cell responses are significantly less polarized when determined ex vivo as compared to those measured after restimulation in vitro. Moreover, the differences in CD4+ T cell proliferation observed between healer and nonhealer strains of mice differed ex vivo and in vitro. Our results suggest that determination of both ex vivo as well as in vitro T cell responses is crucial to characterize immune responses during experimental leishmaniasis.
Highlights
The leishmaniases are a group of vector-borne parasitic diseases that inflict an immense toll in the developing world; they are major causes of morbidity and mortality and impede economic development
Production of the cytokines IFN-γ, IL-4 and IL-10 is strongly amplified after restimulation
In the experimental model of leishmaniasis, immune responses have mostly been characterized by restimulating lymphoid cells from infected mice with Leishmania antigen in vitro [1,2]
Summary
The leishmaniases are a group of vector-borne parasitic diseases that inflict an immense toll in the developing world; they are major causes of morbidity and mortality and impede economic development. These diseases affect an estimated 12 million people in 88 countries, and approximately 350 million people are at risk. Experimental studies in inbred strains of mice with Leishmania (L.) major mimic the healing and nonhealing manifestation of leishmaniasis and have established the current paradigm of T helper (Th) cell subset involvement [1,2,3]. A few strains of mice such as BALB/c develop nonhealing disease, attributed to the expansion of Th2 cells and the production of their signature cytokines interleukin (IL)-4 and IL-13
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