Cutting edge: functional interactions between toll-like receptor (TLR) 2 and TLR1 or TLR6 in response to phenol-soluble modulin.

نویسندگان

  • A M Hajjar
  • D S O'Mahony
  • A Ozinsky
  • D M Underhill
  • A Aderem
  • S J Klebanoff
  • C B Wilson
چکیده

Toll-like receptor (TLR) 2 and TLR4 play important roles in the early, innate immune response to microbial challenge. TLR2 is preferentially involved in the inflammatory response to lipoteichoic acid, lipopeptides, and glycans from a variety of microbes, whereas TLR4 is essential for a complete response to LPSs. We report here that TLR2 transduces the response to phenol-soluble modulin, a factor secreted by Staphylococcus epidermidis. The TLR2-mediated response to this modulin was enhanced by TLR6 but inhibited by TLR1, indicating a functional interaction between these receptors. We also demonstrate that a response to phenol-soluble modulin mediated by TLR2 and TLR6 was more refractory to inhibition by TLR1 than one mediated by TLR2 alone.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Human intestinal epithelial cells are broadly unresponsive to Toll-like receptor 2-dependent bacterial ligands: implications for host-microbial interactions in the gut.

Intestinal epithelial cells (IEC) interact with a high density of Gram-positive bacteria and are active participants in mucosal immune responses. Recognition of Gram-positive organisms by Toll-like receptor (TLR)2 induces proinflammatory gene expression by diverse cells. We hypothesized that IEC are unresponsive to Gram-positive pathogen-associated molecular patterns and sought to characterize ...

متن کامل

P-82: The Role of Toll-Like Receptor 2 in Ectopic Pregnancy

Background: The innate immune system is our first line of defense against invading pathogens. Toll–like receptors (TLRs) have been identified as a key role in mediating the function of innate immune system which bridges the gap between innate and adaptive immunity. For example, TLR2 is able to act as a homodimer to recognize lipoteichoic acids of Gram-positive bacteria but as a heterodimer with...

متن کامل

P-17: Expression of Cell Surface Toll-Like Receptors in the Human Male Reproductive Tract

Background: Male infertility refers to the inability of a male to achieve a pregnancy in a fertile female. The root of many causes of infertility is miscommunication between immune and reproductive system. Male reproductive system is very sensitive and vulnerable, infections can hinder maturation and movement of spermatozoa lead to impaired fertility.All species need an immediate reply to the m...

متن کامل

Cutting edge: distinct Toll-like receptor 2 activators selectively induce different classes of mediator production from human mast cells.

Mast cells play a critical role in host defense against bacterial infection. Murine mast cells produce cytokines in response to bacterial peptidoglycan and LPS via Toll-like receptor (TLR) TLR2- and TLR4-dependent mechanisms. The expression of TLRs by human mast cells and responses to known TLR activators was examined. Human mast cells expressed mRNA for TLR1, TLR2, and TLR6 but not TLR4. Bacte...

متن کامل

Cutting edge: role of Toll-like receptor 1 in mediating immune response to microbial lipoproteins.

The Toll-like receptor (TLR) family acts as pattern recognition receptors for pathogen-specific molecular patterns (PAMPs). TLR2 is essential for the signaling of a variety of PAMPs, including bacterial lipoprotein/lipopeptides, peptidoglycan, and GPI anchors. TLR6 associates with TLR2 and recognizes diacylated mycoplasmal lipopeptide along with TLR2. We report here that TLR1 associates with TL...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Journal of immunology

دوره 166 1  شماره 

صفحات  -

تاریخ انتشار 2001