In:
eLife, eLife Sciences Publications, Ltd, Vol. 3 ( 2014-10-27)
Abstract:
Invasion by a bacterium or virus typically activates a mammalian host's immune system to eliminate the pathogen. The cells of the so-called ‘innate immune system’ are the body's first line of defense against infection, and these cells patrol the organs and tissues in an effort to locate and eliminate pathogens quickly. The innate immune response is rapid and non-specific, but often cannot completely clear an infection. When necessary, innate immune cells will escalate the immune response by activating the second branch of the immune system, called the ‘adaptive immune system’. This specifically targets and eradicates an invading pathogen. T cells are essential components of the adaptive immune system, and these cells can be readily distinguished from other types of cell by proteins called T cell receptors (or TCRs) found on their surface. There are also different types of T cell, each with a specific function. T helper cells, for example, help other adaptive immune cells to mature and activate, which involves these immune cells proliferating and developing into more specialized cells. For a T cell to activate, two events must occur at the same time. First, the TCR must recognize and bind to a fragment of the pathogen that is presented to it by an innate immune cell. And second, ‘co-stimulatory molecules’ present on the surfaces of both the T cell and the same innate immune cell must interact. Using these two signals to activate a T cell helps to ensure the adaptive immune response is not ‘unleashed‘ unnecessarily. Co-stimulatory molecules have become popular targets for therapies aimed at treating autoimmune disorders—where the immune system attacks and destroys the body's own tissues. One of the most well studied co-stimulatory molecules expressed by T cells is called CD28; however, it remained unknown whether CD28 is involved in any processes after T cell activation. Now, Linterman et al. reveal that the CD28 co-stimulatory molecule plays a number of roles in addition to T cell activation. For example, a newly developed mouse model showed that CD28 must remain on the surface of T helper cells after they have been activated for these cells to effectively specialize. Linterman et al. also discovered that CD28 helps different T helper cell subtypes to develop. Linterman et al. demonstrate that CD28 is critical throughout a host's response to infection, and suggest that if CD28 is lost on activated T cells (which happens during aging, HIV infection and autoimmune diseases) the responses of T helper cells become limited. Furthermore, these findings reveal that treatments that target the CD28 co-stimulatory molecule will also affect on-going immune responses.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.03180.001
DOI:
10.7554/eLife.03180.002
DOI:
10.7554/eLife.03180.003
DOI:
10.7554/eLife.03180.004
DOI:
10.7554/eLife.03180.005
DOI:
10.7554/eLife.03180.006
DOI:
10.7554/eLife.03180.007
DOI:
10.7554/eLife.03180.008
DOI:
10.7554/eLife.03180.009
DOI:
10.7554/eLife.03180.010
DOI:
10.7554/eLife.03180.011
DOI:
10.7554/eLife.03180.012
DOI:
10.7554/eLife.03180.013
DOI:
10.7554/eLife.03180.014
DOI:
10.7554/eLife.03180.015
DOI:
10.7554/eLife.03180.016
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2014
detail.hit.zdb_id:
2687154-3
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