Anti- 'CD IND.4' abrogates rejection and restabliches long-term tolerance to sybgenetic newborn hearts grafted in mice chronically infected with trypanosoma cruzi (1992)
- Authors:
- USP affiliated authors: ROSSI, MARCOS ANTONIO - FMRP ; SILVA, JOAO SANTANA DA - FMRP
- Unidades: FMRP; FMRP
- Subjects: PATOLOGIA
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Journal of Experimental Medicine
- Volume/Número/Paginação/Ano: v.175, p.29-39, 1992
-
ABNT
SANTOS, R R; ROSSI, Marcos Antonio; LAUS, J L; et al. Anti- 'CD IND.4' abrogates rejection and restabliches long-term tolerance to sybgenetic newborn hearts grafted in mice chronically infected with trypanosoma cruzi. Journal of Experimental Medicine, New York, v. 175, p. 29-39, 1992. -
APA
Santos, R. R., Rossi, M. A., Laus, J. L., Savino, J. S. S. W., Mengele Junior, J. O., Silva, J. S. da, et al. (1992). Anti- 'CD IND.4' abrogates rejection and restabliches long-term tolerance to sybgenetic newborn hearts grafted in mice chronically infected with trypanosoma cruzi. Journal of Experimental Medicine, 175, 29-39. -
NLM
Santos RR, Rossi MA, Laus JL, Savino JSSW, Mengele Junior JO, Silva JS da, Savino W, Mengel J. Anti- 'CD IND.4' abrogates rejection and restabliches long-term tolerance to sybgenetic newborn hearts grafted in mice chronically infected with trypanosoma cruzi. Journal of Experimental Medicine. 1992 ;175 29-39. -
Vancouver
Santos RR, Rossi MA, Laus JL, Savino JSSW, Mengele Junior JO, Silva JS da, Savino W, Mengel J. Anti- 'CD IND.4' abrogates rejection and restabliches long-term tolerance to sybgenetic newborn hearts grafted in mice chronically infected with trypanosoma cruzi. Journal of Experimental Medicine. 1992 ;175 29-39. - Early dystrophin disruption in the pathogenesis of experimental chronic chagas cardiomyopathy
- Early dystrophin disruption in the pathogenesis of experimental chronic Chagas cardiomyopathy
- nitric oxide synthase-2 modulates chemokine production by Trypanosoma Cruzi-infected cardiac myocytes
- B cell-deficient mice display enhanced susceptibility to Paracoccidioides brasiliensis infection
- Role of interleukin (IL)-18 in experimental paracoccidioidomycosis
- Intercellular adhesion molecule 1 deficieney leads to impaired recruitment of T lymphocytes and enhanced host susceptibility to infection with Trypanosoma cruzi
- Intensification of acute t. Cruzi myocarditis in balb / c nice pretreated
- Permeability alteration of the sarcolemmal membrane particulary at the site of macrophage contact, in experimental chronic trypanosoma cruzi miocarditis in mice
- The left lung is preferentially targeted during experimental paracoccidioidomycosis in C57BL/6 mice
- 5-lipoxygenase activity increases susceptibility to experimental paracoccidioides brasiliensis infection
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