RESUMEN
In the present study, we investigated whether natural killer (NK) cells modulate immunoglobulin (Ig) secretion by B cells from Trypanosoma cruzi-infected mice. B cells from infected mice increased IgM and IgG2a secretion in the presence of a NK cell line, and this response was cell contact-dependent. Stimulation of splenic B cells with polyinosinic-polycytidylic acid, a NK cell activator, also increased Ig secretion by B cells from infected mice. B cells from infected mice expressed higher levels of the B7.2 molecule. Our results suggest that NK cells may be involved in the control of the abnormal B cell activation observed during T. cruzi infection.
Asunto(s)
Anticuerpos Antiprotozoarios/análisis , Linfocitos B/inmunología , Enfermedad de Chagas/inmunología , Trypanosoma cruzi/inmunología , Animales , Antígenos CD/análisis , Linfocitos B/efectos de los fármacos , Antígeno B7-2 , Células Cultivadas , Ensayo de Inmunoadsorción Enzimática , Femenino , Citometría de Flujo , Inmunoglobulina G/análisis , Inmunoglobulina M/análisis , Células Asesinas Naturales/inmunología , Lipopolisacáridos/farmacología , Activación de Linfocitos , Masculino , Glicoproteínas de Membrana/análisis , Ratones , Ratones Endogámicos BALB C , Poli I-C/farmacologíaRESUMEN
Glycoinositolphospholipids (GIPLs) are some of the major glycolipids of the Trypanosoma cruzi surface that were previously shown to activate B cells. In the present study, we investigated whether (i) T. cruzi GIPLs could induce immunoglobulin secretion from B cells in the absence of T cells and NK cells and whether (ii) NK cells are also stimulated by the GIPLs. B cells purified from mice deficient in both T and NK cells (CD3epsilon transgenic mice) secreted immunoglobulin in response to the GIPL. This response was increased by coculture with a murine NK cell line. The T. cruzi GIPL also increased the NK cell (interleukin-2 induced) proliferative response. Our data indicate that the T. cruzi GIPL has a direct stimulatory effect on NK cells and induces immunoglobulin secretion in the absence of T lymphocytes and NK cells. These findings suggest that this T. cruzi-derived molecule may be one of the stimulators that lead to NK cell activation during T. cruzi infection.