Signaling Organelles of the Innate Immune System

نویسنده

  • Jonathan C. Kagan
چکیده

There are at least five families of microbe-detection receptors that function to detect and eradicate potentially infectious microorganisms that enter multicellular eukaryotes. While a multitude of proteins regulating innate immune signal transduction have already been defined, continuous genetic screening for regulators of innate immunity may not yield as significant insight into the operation of these pathways as was obtained in the past. This diminished return on experimental investment suggests that we are approaching the asymptote of genetics-only approaches to study innate immunity. In contrast, it remains unclear how known regulators of innate immunity interact within the infrastructure of mammalian cells to execute their signaling functions. In this Perspective, I first highlight the locations within mammalian cells that permit innate immune signal transduction and then offer a model whereby structurally distinct proteins can be grouped functionally through their ability to assemble platforms of regulators on the signaling organelles of the innate immune system.

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

Autophagy as an Innate Immune Modulator

Autophagy is a fundamental cellular process in eukaryotic cells for maintaining homeostasis by degrading cellular proteins and organelles. Recently, the roles of autophagy have been expanded to immune systems, which in turn modulate innate immune responses. More specifically, autophagy acts as a direct effector for protection against pathogens, as well as a modulator of pathogen recognition and...

متن کامل

A Promiscuous Lipid-Binding Protein Diversifies the Subcellular Sites of Toll-like Receptor Signal Transduction

The Toll-like receptors (TLRs) of the innate immune system are unusual in that individual family members are located on different organelles, yet most activate a common signaling pathway important for host defense. It remains unclear how this common signaling pathway can be activated from multiple subcellular locations. Here, we report that, in response to natural activators of innate immunity,...

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

Sliver nanoparticles accelerate skin wound healing in mice (Mus musculus) through suppression of innate immune system

Objective(s): This study aimed to find the effects of silver nanoparticles (Ag-NPs) (40 nm) on skin wound healing in mice Mus musculus when innate immune system has been suppressed.Materials and Methods: A group of 50 BALB/c mice of about 8 weeks (weighting 24.2±3.0 g) were randomly divided into two groups: Ag-NPs and control group, each with 25 mice. Once a day at the same time, a volume of 50...

متن کامل

P-184: The Role of Cell Surface Toll Like Receptors in Endometriosis

Background: Toll like receptors (TLRs) are a major family of innate immune systems which recognize specific pathogen associated molecular patterns (PAMPS)in bacterial, fungi, virus and parasites. Human TLRs comprise a large family of 10 different type proteins that are expressed on various immune cells. Among these receptors, TLR1, 2, 4, 5, 6 and 10 were expressed on the cell surface. TLR2 form...

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:
  • Cell

دوره 151  شماره 

صفحات  -

تاریخ انتشار 2012