SOCS3 expression induced by PIM2 requires PKC and PI3K signaling |
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Authors: | Yeddula Narayana Kushagra Bansal Akhauri Yash Sinha Nisha Kapoor Germain Puzo Martine Gilleron Kithiganahalli Narayanaswamy Balaji |
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Affiliation: | aDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, India;bDepartment of Molecular Mechanisms of Mycobacterial Infections, Institut de Pharmacologie et de Biologie Structurale du Centre National de la Recherche Scientifique (CNRS) and Université Paul Sabatier, 205 route de Narbonne, 31077 Toulouse Cedex 4, France |
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Abstract: | Initiation of proinflammatory host immunity in response to infection represents as a key event in effective control and containment of the pathogen at the site of infection as well as in elicitation of robust immune memory responses. In the current investigation, we demonstrate that an integral cell wall antigen of the mycobacterial envelope, Phosphatidyl-myo-inositol dimannosides (PIM2) triggers Suppressor of cytokine signaling (SOCS) 3 expression in macrophages in a Toll-like receptor 2 (TLR2)-MyD88 dependent manner. Data derived from signaling perturbations suggest the involvement of phosphoinositide-3 kinase (PI3K) and protein kinase C (PKC) signaling pathways during PIM2 induced SOCS3 expression. Further, pharmacological inhibition of ERK1/2, but not of p38 MAP kinase or JNK abrogated the induced expression of SOCS3. The PIM2 induced activation of ERK1/2 was dependent on the activation of PI3K or PKC signaling which in turn regulated p65 nuclear factor -κB (NF-κB) nuclear translocation. Overall, current study delineates the role for PI3K-PKC axis and ERK1/2 signaling as key signaling events during PIM2 induced SOCS3 expression in macrophages. |
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Keywords: | PIM2 TLR2 SOCS3 PI3K PKC |
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