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Titolo:
LEISHMANIA-MAJOR INFECTION IN MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II-DEFICIENT MICE - CD8(-CELLS DO NOT MEDIATE A PROTECTIVE IMMUNE-RESPONSE() T)
Autore:
ERB K; BLANK C; RITTER U; BLUETHMANN H; MOLL H;
Indirizzi:
MALAGHAN INST MED RES,POB 7060 WELLINGTON NEW ZEALAND UNIV WURZBURG,RES CTR INFECT DIS WURZBURG GERMANY F HOFFMANN LA ROCHE & CO LTD,PHARMACEUT RES GENE TECHNOL BASEL SWITZERLAND
Titolo Testata:
Immunobiology
fascicolo: 2, volume: 195, anno: 1996,
pagine: 243 - 260
SICI:
0171-2985(1996)195:2<243:LIIMHC>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
MURINE CUTANEOUS LEISHMANIASIS; SUSCEPTIBLE BALB/C MICE; TUMOR-NECROSIS-FACTOR; KNOCK-OUT MICE; INTERFERON-GAMMA; NUDE-MICE; MONOCLONAL-ANTIBODY; TH1 CELLS; RESISTANCE; INTERLEUKIN-4;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
K. Erb et al., "LEISHMANIA-MAJOR INFECTION IN MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II-DEFICIENT MICE - CD8(-CELLS DO NOT MEDIATE A PROTECTIVE IMMUNE-RESPONSE() T)", Immunobiology, 195(2), 1996, pp. 243-260

Abstract

In order to evaluate the role of CD8(+) T cells in cutaneous leishmaniasis, major histocompatibility complex (MHC) class II-deficient mice of C57BL/6 background lacking functional CD4(+) T cells were infected with Leishmania major. In contrast to C57BL/6 wild-type mice which areresistant to infection with L. major, these mice developed severe skin lesions that did not heal. In comparison to susceptible BALB/c mice,however, lesion development in MHC class II-deficient mice was very much retarded, even though the increase in the parasite load in lymphoid organs was only slightly delayed. Lymph node cells from L. major-infected MHC class II-deficient mice produced very low levels of interferon-gamma upon stimulation with L. major antigen, whereas the response to the mitogen concanavalin A was not impaired. Interestingly, they did not release lymphokines associated with disease exacerbation (interleukin 4 and interleukin 10) either, suggesting that the delayed lesiondevelopment is caused by the lack of disease-promoting CD4(+) cells rather than by the presence of protective CD8(+) cells. The lack of L. major-reactive immunoglobulins in the serum of infected MHC class II-deficient mice indicates that B cells also cannot respond to parasite antigens in the absence of MHC class II-mediated helper signals. The data demonstrate that MHC class II-deficient mice are unable to restrictthe spreading of L. major, although they contain highly increased proportions of CD8(+) T cells. Thus, MHC class II-restricted immune responses, most likely mediated by functional CD4(+) T cells, are essentialfor the control of primary infections with L. major.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 05:56:56