Immune Responses of IL‐4, IL‐5, IL‐6 Deficient Mice

Köpf, Manfred; Gros, Graham Le; Coyle, Anthony J.; Kosco-Vtlbois, Marie; Brombacher, Frank; Köhler, Georges

doi:10.1111/j.1600-065x.1995.tb00093.x

Cited by 132 publications

(69 citation statements)

References 116 publications

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“…We found that expression levels of IL-6 and a chemokine CCL5 are markedly lower in stimulated HSF1-null spleen cells than those in wild-type mice. IL-6 is a multifunctional cytokine that regulates the immune response and inflammation (24,31). During an antibody response dependent on T cell help, IL-6 is secreted by a germinal center cells and promotes expansion of plasma blasts.…”

Section: Discussionmentioning

confidence: 99%

Impaired IgG Production in Mice Deficient for Heat Shock Transcription Factor 1

Inouye¹,

Izu²,

Takaki³

et al. 2004

Journal of Biological Chemistry

102

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Heat shock factor 1 (HSF1) is a major transactivator of heat shock proteins in response to heat shock, and it is also involved in oogenesis, spermatogenesis, and placental development. However, we do not know the molecular mechanisms controlling developmental processes. In this study, we found that HSF1-null mice exhibited a significant decrease in the T cell-dependent B cell response. When mice were immunized intraperitoneally with sheep red blood cells, the sheep red blood cellspecific IgG production, especially IgG2a production, in HSF1-null mice was about 50% lower than that in wildtype mice at 6 days after the immunization, whereas IgM production was normal. The number of bromodeoxyuridine-incorporated spleen cells in immunized HSF1-null mice was one-third that in immunized wild-type mice, indicating reduced proliferation of the spleen cells. We analyzed levels of cytokines and chemokines in spleen cells and in peritoneal macrophages stimulated with lipopolysaccharide and interferon-␥ and found that expression levels of interleukin-6 and CCL5 were significantly lower in HSF1-null cells than those in wild-type cells. Furthermore, we demonstrated that the IL-6 gene is a direct target gene of HSF1. These results revealed a novel molecular link between HSF1 and a gene related to immune response and inflammation.

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Section: Discussionmentioning

confidence: 99%

Impaired IgG Production in Mice Deficient for Heat Shock Transcription Factor 1

Inouye¹,

Izu²,

Takaki³

et al. 2004

Journal of Biological Chemistry

102

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“…IL-6 was originally identified as a lymphokine inducing final maturation of B cells into antibody-secreting cells [a, 31,321. Consequently, IL-6-deficient mice exhibit reduced antibody levels and impaired antibody responses [13,14,151. Measurements of serum levels of IgM-and IgG antibodies against ICC membrane antigens in our own experiments demonstrate a lack of increase in xenoreactive antibodies in IL-6-deficient mice after ICC xenotransplantation, corresponding to levels seen in wild-type controls.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-6 in islet xenograft rejection

Benda

Korsgren

2001

Transplant International

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Earlier work on primate cardiac xenotransplantation has demonstrated a correlation between interleukin (1L)-6 levels and severity of vascular rejection. IL-6 was originally identified as a lymphokine inducing final maturation of B lymphocytes into antibody-secreting cells. The present study aimed to evaluate the role of IL-6 in fetal porcine islet-like cell cluster (ICC) xenograft rejection. Moreover, other authors have reported that eosinophils dominate the cellular response following discordant islet xenograft transplantation. Here, a technique for specific detection of eosinophils was applied. IL-6-deficient mice and wild-type controls were implanted with fetal porcine ICCs under the kidney capsule and killed 4-, 7-, and 10 days after transplantation. Xenografts were histologically evaluated, and serum samples were analyzed for IgM and IgG antibodies against ICC membrane antigens. IL-6-deficient mice and wild-type controls readily rejected the xenograft. On day 7 after transplantation, abundant numbers of F4/ 80' and Mac-l+ cells were found distributed throughout the collapsing graft accompanied by small amounts of eosinophils and peripherally accumulated CD3' T cells (predominantly CD4'). Significantly lower serum levels of IgM and IgG antibodies against ICC membrane antigens were observed in IL-6-deficient mice on day 4 or 7 after transplantation when compared to wild-type controls. No significant differences were seen on day 10 after transplantation. In both experimental groups, specific IgM and IgG antibody levels remained stable over time. In the pig-to-mouse model, IL-6 seems to be of minor importance to fetal porcine ICC xenograft rejection. Macrophages, and not eosinophils, dominate the cellular response associated with this process.

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“…[21][22][23][24][25] We describe a linkage of serum IgE level to loci on chromosomes 10 and 5, near D10Mit25 and D5Mit112, respectively. A number of loci controlling IgE level have been described in humans (reviewed in Holgate 26 ) including the cytokine cluster on human chromosome 5.…”

Section: Discussionmentioning

confidence: 99%

Susceptibility to Leishmania major infection in mice: multiple loci and heterogeneity of immunopathological phenotypes

et al. 2000

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Susceptibility as opposed to resistance of mouse strains (eg, BALB/c vs C57BL/6) to Leishmania major has been attributed to a defective Th1 and a predominant Th2-response, resulting in increased IL-4 and IgE production, and decreased interferon gamma (IFN␥) production, macrophage activation and elimination of parasites. Here we report dissection of genetic and functional aspects of susceptibility to leishmaniasis using two contrasting inbred strains BALB/cHeA (susceptible) and STS/A (resistant) and a resistant Recombinant Congenic (RC) Strain, CcS-5/Dem, which carries a random set of 12.5% of genes from the strain STS and 87.5% genes from the susceptible strain BALB/c. Linkage analysis of F 2 hybrids between the resistant RC strain CcS-5 and the susceptible strain BALB/c revealed five loci affecting the response to the infection, each apparently associated with a different combination of pathological symptoms and immunological reactions. The correlation between Th2-type immune reactions and the disease in the F 2 mice was either absent, or it was limited to mice with specific genotypes at loci on chromosomes 10 and 17. This suggests that the resistance vs susceptibility is influenced by mechanisms additional to the postulated antagonistic effects of Th1 and Th2 responses, and that the host's genotype affects the development of leishmaniasis in a complex way. Genes and Immunity (2000) 1, 200-206.

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Immune Responses of IL‐4, IL‐5, IL‐6 Deficient Mice

Cited by 132 publications

References 116 publications

Impaired IgG Production in Mice Deficient for Heat Shock Transcription Factor 1

Impaired IgG Production in Mice Deficient for Heat Shock Transcription Factor 1

Interleukin-6 in islet xenograft rejection

Susceptibility to Leishmania major infection in mice: multiple loci and heterogeneity of immunopathological phenotypes

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