Calendar

Publication date: 2 June 2017
Source:Polymer, Volume 118





http://ift.tt/2qzJXOi

Reply

Publication date: Available online 18 May 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Peter K. Smith, Madhan Masilamani, Xiu-Min Li, Hugh A. Sampson




http://ift.tt/2ry8mAX

Polyfunctionality of bona fide resident lung CD69+ natural killer cells

Publication date: Available online 18 May 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Baptiste Hervier, Isabelle Cremer, Vincent Vieillard




http://ift.tt/2qzCJK6

Reply

Publication date: Available online 18 May 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Nicole Marquardt, Hans-Gustaf Ljunggren, Jakob Michaëlsson




http://ift.tt/2ryiLwQ

Additional effects of dietary advanced glycation end products

Publication date: Available online 18 May 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Jeffrey D. Miller




http://ift.tt/2qzSQHM

Cockroach Allergy and Urban Asthma

Publication date: Available online 19 May 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Peyton A. Eggleston




http://ift.tt/2ryfzRK

Heterotrimeric complex of p38 MAPK, PKCδ, and TIRAP is required for AP1 mediated inflammatory response

Publication date: July 2017
Source:International Immunopharmacology, Volume 48
Author(s): Mirza S. Baig, Dongfang Liu, Kannan Muthu, Anjali Roy, Uzma Saqib, Adnan Naim, Syed M. Faisal, Mansi Srivastava, Rohit Saluja
Inflammation could be described as a physiological response of the body to tissue injury, pathogen invasion, and irritants. During the inflammatory phase, cells of both the innate as well as adaptive immune system are activated and recruited to the site of inflammation. These mediators are downstream targets for the transcription factors; activator protein-1 (AP1), nuclear factor kappa-light-chain-enhancer (NF-κB), signal transducers and activators of transcription factors (STAT1), as well as interferon regulatory factors (IRFs), which control the expression of most immunomodulatory genes.There is a significant increase in active p38 mitogen-activated protein kinase (p38MAK) immediately after lipopolysaccharide (LPS) stimulation, which results in the activation of AP-1 transcription factor and expression of proinflammatory cytokines, IL-12 and IL-23. We studied the novel mechanism of p38 MAPK activation through the formation of a heterotrimeric complex of Protein kinase C delta type (PKCδ), Toll-Interleukin 1 Receptor (TIR) Domain Containing Adaptor Protein (TIRAP), and p38 proteins. TIRAP serves as an adaptor molecule which brings PKCδ and p38 in close proximity. The complex facilitates the activation of p38MAPK by PKCδ.Therefore, we propose that disruption of the heterotrimeric complex may be a good strategy to dampen the inflammatory response. Structure-based design of small molecules or peptides targetting PKCδ-TIRAP or TIRAP-p38 interfaces would be beneficial for therapy in AP1 mediated inflammatory diseases.



http://ift.tt/2qzPW5G