INVESTIGADORES
MALCHIODI Emilio Luis
artículos
Título:
Different Trypanosoma cruzi strains promote neuromyopathic damage mediated by
Autor/es:
MIRKIN GA, CELENTANO AM, MALCHIODI EL, JONES M, GONZÁLEZ CAPPA SM.
Revista:
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
Referencias:
Año: 1997 vol. 107 p. 328 - 334
ISSN:
0009-9104
Resumen:
The proliferative response of CD4 and CD8 T lymphocytes obtained from C3H/HeNmice chronically infected with Trypanosoma cruzi strains that differ invirulence, tropism and immunogenicity, was assayed against skeletal muscle,sciatic nerve and spinal cord homogenates. Although both CD4 and CD8 Tlymphocytes from mice infected with the RA strain strongly proliferated againstthe nervous system, no response against skeletal muscle antigens was detected.CD4 and CD8 T lymphocytes from mice infected with the K-98 clone (from CA-Istrain) showed low proliferative response against all the antigens assayed. Todetermine whether the proliferation patterns showed correlation with Tcell-mediated neuromuscular damage, passive cell transfer studies were performed.Fifteen days after transfer of CD4 T cells from RA-infected donors (CD4-RA),normal syngeneic recipients displayed exclusively nervous tissue damage, such as perineural, endoneural and/or meningeal inflammatory infiltrates, withpredominance of CD4 T cells. Fifteen days after transfer of CD4 T lymphocytesfrom mice infected with K-98 (CD4-K98), recipients showed inflammatoryinfiltrates only in skeletal muscle, where CD4 T lymphocytes and macrophages werepredominant cells. Recipients of CD8 T cells from RA-infected mice (CD8-RA)showed lesions in both spinal cord and sciatic nerves. Higher percentages of CD8 T cells were observed in comparison with the recipients of CD4-RA or CD4-K98. In contrast, CD8 T cells from K-98-infected donors (CD8-K98) did not induce tissuedamage. These results provide evidence that mice infected with T. cruzipopulations that differ in their biological characteristics show diverse immunemechanisms that may be involved in the pathogenesis of peripheral nervous system damage.