Also Included In: Dermatology; HIV / AIDS; Transplants / Organ Donations
Article Date: 13 Dec 2011 - 1:00 PST
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IMMUNOLOGY: Finding a new immune function for NEMO
Ectodermal dysplasias are a group of inherited conditions in which there is abnormal development and function of the skin, hair, nails, teeth, and/or sweat glands. Individuals with ectodermal dysplasia with immune deficiency (EDI) also have a dysfunctional immune system that renders them susceptible to severe infections. EDI is caused by mutations in the NEMO gene that reduce but do not abolish expression of NEMO protein. Now, a team of researchers led by Ashish Jain, at the National Institute of Allergy and Infectious Diseases, Bethesda, has identified two patients with EDI caused by genetic mutations that are not within the NEMO gene but do markedly reduce the level of expression of NEMO. Detailed analysis of cells from these patients defined a new and unexpected function for NEMO - it controls the activity of the protein IKK-alpha in the nucleus. Importantly, the data indicate that defects in this function of NEMO result in the immune deficiency that is characteristic of EDI.
TITLE: Defective nuclear IKK-alpha function in patients with ectodermal dysplasia with immune deficiency
View this article at: http://www.jci.org/articles/view/42534?key=05ee401b0eeda41b75be
IMMUNOLOGY: Putting a stop to immune responses
To clear an invading microbe from the body the immune system must become activated. However, once the microbe has been cleared it is important to shut down the immune response so that it does not cause damage to healthy tissue surrounding the site of infection. In some instances, suppression of the immune response occurs before the immune system has done its job. For example, many tumors contain cells known as MDSCs that suppress antitumor immune responses. A team of researchers led by Leo Koenderman, at the University Medical Center Utrecht, The Netherlands, has now identified in humans a new population of immune system-suppressing cells characterized by high levels of expression of the proteins CD11c, CD11b, and CD16 and low levels of expression of the protein CD62L. The cells were observed in humans during acute body-wide inflammation induced by injection of a bacteria-derived toxin or by severe injury. Further analysis identified the mechanisms by which these cells suppressed the immune system, providing potential targets for preventing unwanted immune system suppression.
TITLE: A subset of neutrophils in human systemic inflammation inhibits T cell responses through Mac-1
View this article at: http://www.jci.org/articles/view/57990?key=ffff831d2c7a509bd694
IMMUNOLOGY: Numbers of immune first responders kept constant by LXRs
One of the first immune cells to respond to an invading microbe is the neutrophil. Numbers of these cells are tightly regulated because of their importance as a first responder. In healthy individuals, more than 1 - 109 neutrophils per kilogram body weight are released from the bone marrow every day; an equivalent number must be cleared from the circulation to ensure numbers remain constant. A team of researchers - led by Steven Bensinger and Peter Tontonoz, at UCLA, Los Angeles - has now determined that proteins known as LXRs are key regulators of neutrophil clearance and production in mice and identified the molecular pathways by which the LXRs do so. As dysregulation of neutrophil clearance has been implicated in the development of lupus, future studies will focus on determining whether modulating LXR signaling can modify disease in animal models of lupus.
TITLE: Coordinate regulation of neutrophil homeostasis by liver X receptors in mice
View this article at: http://www.jci.org/articles/view/58393?key=abc382b18a21deb76dfb
HIV/AIDS; Recruitment (of CD4+ T cells) a problem for the gut
HIV-1 infection is characterized by the loss of key immune cells known as CD4+ T cells. Combined antiretroviral therapy (cART) largely restores CD4+ T cell numbers in the blood, but the gut remains substantially depleted of these cells. A team of researchers led by Pierre Delobel, at INSERM, UMR1043, France, has now determined that the inefficient restoration of CD4+ T cell numbers in the gut of cART-treated HIV-infected individuals is likely to be a result of a lack of recruitment of CD4+ T cells; in particular, those CD4+ T cells that express the proteins CCR9 and beta-7. Moreover, this is probably because expression of the molecule CCL25, which attracts CD4+ T cells expressing the protein CCR9, is decreased in the small intestine of HIV-infected individuals. These data provide a potential explanation for the inefficient restoration of gut CD4+ T cell numbers in HIV-infected individuals receiving effective cART, something that was poorly understood.
TITLE: Altered CD4+ T cell homing to the gut impairs mucosal immune reconstitution in treated HIV-infected individuals
View this article at: http://www.jci.org/articles/view/59011?key=a0a1ec7e537acfb05110
TRANSPLANTATION: The protein haptoglobin: arising from dead cells to trigger graft rejection
The process of transplanting an organ is complex. Despite great care, some cells of the organ die during the harvesting and implantation procedures. These dead cells activate a branch of the organ recipient's immune system known as the innate immune system. This impairs the ability of the organ recipient's immune system to tolerate the new organ, which can lead to rapid rejection of the transplanted organ (acute transplant rejection). A team of researchers led by Daniel Goldstein, at Yale University School of Medicine, New Haven, has now determined that release of the protein haptoglobin from dying skin cells activates the innate immune system and accelerates transplant rejection in a mouse model of skin transplantation. As there are three major variants of haptoglobin in humans, Goldstein and colleagues suggest that it would be interesting to determine whether differential expression of these haptoglobin variants influences rejection of transplanted hearts in humans.
TITLE: Haptoglobin activates innate immunity to enhance acute transplant rejection in mice
View this article at: http://www.jci.org/articles/view/58344?key=68e86efe8058c7046e4b
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.Visit our immune system / vaccines section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:
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13 Dec. 2011.
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