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MyD88-dependent signaling contributes to protection following Bacillus anthracis spore challenge of mice: implications for Toll-like receptor signaling.

Hughes MA, Green CS, Lowchyj L, Lee GM, Grippe VK, Smith MF Jr, Huang LY, Harvill ET, Merkel TJ.

Infect Immun. 2005 Nov;73(11):7535-40.


Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent.

Huang LY, Aliberti J, Leifer CA, Segal DM, Sher A, Golenbock DT, Golding B.

J Immunol. 2003 Aug 1;171(3):1441-6.


The Poly-γ-d-Glutamic Acid Capsule Surrogate of the Bacillus anthracis Capsule Is a Novel Toll-Like Receptor 2 Agonist.

Jeon JH, Lee HR, Cho MH, Park OK, Park J, Rhie GE.

Infect Immun. 2015 Oct;83(10):3847-56. doi: 10.1128/IAI.00888-15.


Role of Bacillus anthracis spore structures in macrophage cytokine responses.

Basu S, Kang TJ, Chen WH, Fenton MJ, Baillie L, Hibbs S, Cross AS.

Infect Immun. 2007 May;75(5):2351-8.


Involvement of TLR2 in innate response to Bacillus anthracis infection.

Weiss S, Levy H, Fisher M, Kobiler D, Altboum Z.

Innate Immun. 2009 Feb;15(1):43-51. doi: 10.1177/1753425908100379.


Murine splenocytes produce inflammatory cytokines in a MyD88-dependent response to Bacillus anthracis spores.

Glomski IJ, Fritz JH, Keppler SJ, Balloy V, Chignard M, Mock M, Goossens PL.

Cell Microbiol. 2007 Feb;9(2):502-13.


Containment of aerogenic Mycobacterium tuberculosis infection in mice does not require MyD88 adaptor function for TLR2, -4 and -9.

Hölscher C, Reiling N, Schaible UE, Hölscher A, Bathmann C, Korbel D, Lenz I, Sonntag T, Kröger S, Akira S, Mossmann H, Kirschning CJ, Wagner H, Freudenberg M, Ehlers S.

Eur J Immunol. 2008 Mar;38(3):680-94. doi: 10.1002/eji.200736458.


The role of MyD88 and TLR4 in the LPS-mimetic activity of Taxol.

Byrd-Leifer CA, Block EF, Takeda K, Akira S, Ding A.

Eur J Immunol. 2001 Aug;31(8):2448-57.


Differential induction of the toll-like receptor 4-MyD88-dependent and -independent signaling pathways by endotoxins.

Zughaier SM, Zimmer SM, Datta A, Carlson RW, Stephens DS.

Infect Immun. 2005 May;73(5):2940-50. Erratum in: Infect Immun. 2006 May;74(5):3077.


The MyD88-dependent, but not the MyD88-independent, pathway of TLR4 signaling is important in clearing nontypeable haemophilus influenzae from the mouse lung.

Wieland CW, Florquin S, Maris NA, Hoebe K, Beutler B, Takeda K, Akira S, van der Poll T.

J Immunol. 2005 Nov 1;175(9):6042-9.


Macrophage-specific TLR2 signaling mediates pathogen-induced TNF-dependent inflammatory oral bone loss.

Papadopoulos G, Weinberg EO, Massari P, Gibson FC 3rd, Wetzler LM, Morgan EF, Genco CA.

J Immunol. 2013 Feb 1;190(3):1148-57. doi: 10.4049/jimmunol.1202511.


MyD88 and TLR2, but not TLR4, are required for host defense against Cryptococcus neoformans.

Biondo C, Midiri A, Messina L, Tomasello F, Garufi G, Catania MR, Bombaci M, Beninati C, Teti G, Mancuso G.

Eur J Immunol. 2005 Mar;35(3):870-8.


The development of early host response to Pseudomonas aeruginosa lung infection is critically dependent on myeloid differentiation factor 88 in mice.

Power MR, Peng Y, Maydanski E, Marshall JS, Lin TJ.

J Biol Chem. 2004 Nov 19;279(47):49315-22. Erratum in: J Biol Chem. 2005 Jan 21;280(3):2395-6.


Toll-like receptor 2 mediates inflammatory cytokine induction but not sensitization for liver injury by Propioni- bacterium acnes.

Romics L Jr, Dolganiuc A, Velayudham A, Kodys K, Mandrekar P, Golenbock D, Kurt-Jones E, Szabo G.

J Leukoc Biol. 2005 Dec;78(6):1255-64.


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