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Gene Review

Myd88  -  myeloid differentiation primary response...

Mus musculus

Synonyms: Myeloid differentiation primary response protein MyD88
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Disease relevance of Myd88


High impact information on Myd88

  • Myd88(-/-) and Tlr4(-/-)Tlr2(-/-) mice showed impaired transepithelial migration of inflammatory cells but decreased survival and enhanced epithelial cell apoptosis after lung injury [3].
  • TLR signaling via the Myd88 adaptor protein drove differentiation of myeloid progenitors, bypassing some normal growth and differentiation requirements, and also drove lymphoid progenitors to become dendritic cells [4].
  • In WT and Myd88(-/-) mice, Ptgs2 was expressed in scattered mesenchymal cells [5].
  • Myd88-dependent positioning of Ptgs2-expressing stromal cells maintains colonic epithelial proliferation during injury [5].
  • These findings demonstrate that Myd88 and prostaglandin signaling pathways interact to preserve epithelial proliferation during injury using what we believe to be a previously undescribed mechanism requiring proper cellular mobilization within the crypt niche [5].

Biological context of Myd88


Anatomical context of Myd88

  • Myd88-dependent in vivo maturation of splenic dendritic cells induced by Leishmania donovani and other Leishmania species [8].
  • The differential role of MyD88 may represent one mechanism by which macrophages regulate innate responses specific to different pathogenic fungi [6].
  • Neutrophilia was completely restored by transferring wild-type bone marrow-derived mast cells into MyD88(-/-) or W/W(v) mice [9].
  • The residual 20% neutrophil infiltration seen in mast cell-deficient and MyD88(-/-) mice was not further reduced by thioperamide [9].
  • However, in response to a TLR4 ligand, lipopolysaccharide (LPS), MyD88-deficient (MyD88(-/-)) DC can up-regulate co-stimulatory molecule expression and enhance their T cell stimulatory activity, indicating that the MyD88-independent pathway through TLR4 can induce some features of DC maturation [7].

Associations of Myd88 with chemical compounds

  • In this study, we have further characterized function of LPS-stimulated, MyD88(-/-) DC [7].

Regulatory relationships of Myd88

  • In contrast, in response to LPS, MyD88(-/-) DC augmented their ability to induce IL-4 instead of IFN-gamma in alloMLR [7].

Other interactions of Myd88

  • Consistently, Irf7-/- mice are more vulnerable than Myd88-/- mice to viral infection, and this correlates with a marked decrease in serum IFN levels, indicating the importance of the IRF-7-dependent induction of systemic IFN responses for innate antiviral immunity [10].
  • Impaired production of T(h)1-inducing cytokines in MyD88(-/-) DC cannot fully account for their increased T(h)2 cell-supporting ability, because absence of T(h)1-inducing cytokines in DC caused impairment of IFN-gamma, but did not lead to augmentation of IL-4 production in alloMLR [7].
  • Cytokine production by MyD88(-/-) macrophages in response to C. albicans yeasts and hyphae was substantially decreased, but responses to A. fumigatus hyphae were preserved [6].


  1. Mechanism of pathogen-specific TLR4 activation in the mucosa: fimbriae, recognition receptors and adaptor protein selection. Fischer, H., Yamamoto, M., Akira, S., Beutler, B., Svanborg, C. Eur. J. Immunol. (2006) [Pubmed]
  2. Pathological role of Toll-like receptor signaling in cerebral malaria. Coban, C., Ishii, K.J., Uematsu, S., Arisue, N., Sato, S., Yamamoto, M., Kawai, T., Takeuchi, O., Hisaeda, H., Horii, T., Akira, S. Int. Immunol. (2007) [Pubmed]
  3. Regulation of lung injury and repair by Toll-like receptors and hyaluronan. Jiang, D., Liang, J., Fan, J., Yu, S., Chen, S., Luo, Y., Prestwich, G.D., Mascarenhas, M.M., Garg, H.G., Quinn, D.A., Homer, R.J., Goldstein, D.R., Bucala, R., Lee, P.J., Medzhitov, R., Noble, P.W. Nat. Med. (2005) [Pubmed]
  4. Toll-like receptors on hematopoietic progenitor cells stimulate innate immune system replenishment. Nagai, Y., Garrett, K.P., Ohta, S., Bahrun, U., Kouro, T., Akira, S., Takatsu, K., Kincade, P.W. Immunity (2006) [Pubmed]
  5. Myd88-dependent positioning of Ptgs2-expressing stromal cells maintains colonic epithelial proliferation during injury. Brown, S.L., Riehl, T.E., Walker, M.R., Geske, M.J., Doherty, J.M., Stenson, W.F., Stappenbeck, T.S. J. Clin. Invest. (2007) [Pubmed]
  6. Differential role of MyD88 in macrophage-mediated responses to opportunistic fungal pathogens. Marr, K.A., Balajee, S.A., Hawn, T.R., Ozinsky, A., Pham, U., Akira, S., Aderem, A., Liles, W.C. Infect. Immun. (2003) [Pubmed]
  7. Endotoxin can induce MyD88-deficient dendritic cells to support T(h)2 cell differentiation. Kaisho, T., Hoshino, K., Iwabe, T., Takeuchi, O., Yasui, T., Akira, S. Int. Immunol. (2002) [Pubmed]
  8. Myd88-dependent in vivo maturation of splenic dendritic cells induced by Leishmania donovani and other Leishmania species. De Trez, C., Brait, M., Leo, O., Aebischer, T., Torrentera, F.A., Carlier, Y., Muraille, E. Infect. Immun. (2004) [Pubmed]
  9. Critical role of histamine H4 receptor in leukotriene B4 production and mast cell-dependent neutrophil recruitment induced by zymosan in vivo. Takeshita, K., Sakai, K., Bacon, K.B., Gantner, F. J. Pharmacol. Exp. Ther. (2003) [Pubmed]
  10. IRF-7 is the master regulator of type-I interferon-dependent immune responses. Honda, K., Yanai, H., Negishi, H., Asagiri, M., Sato, M., Mizutani, T., Shimada, N., Ohba, Y., Takaoka, A., Yoshida, N., Taniguchi, T. Nature (2005) [Pubmed]
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