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Results for “Immune function”

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At least 1,369 records · Page 76Linked to original sources
PubMed1999

Effects of space flight and IGF-1 on immune function.

We tested the hypothesis that insulin-like growth factor-1 (IGF-1) would ameliorate space flight-induced effects on the immune system. Twelve male, Sprague-Dawley rats, surgically implanted with mini osmotic pumps, were subjected to space flight for 10 days on STS-77. Six rats received 10 mg/kg/day of IGF-1 and 6 rats received saline. Flight animals had a lymphocytopenia and granulocytosis which were reversed by IGF-1. Flight animals had significantly higher corticosterone levels than ground controls but IGF-1 did not impact this stress hormone. Therefore, the reversed granulocytosis did not correlate with serum corticosterone. Space flight and IGF-1 also combined to induce a monocytopenia that was not evident in ground control animals treated with IGF-1 or in animals subjected to space flight but given physiological saline. There was a significant increase in spleen weights in vivarium animals treated with IGF-1, however, this change did not occur in flight animals. We observed reduced agonist-induced lymph node cell proliferation by cells from flight animals compared to ground controls. The reduced proliferation was not augmented by IGF-1 treatment. There was enhanced secretion of TNF, IL-6 and NO by flight-animal peritoneal macrophages compared to vivarium controls, however, O2(-) secretion was not affected. These data suggest that IGF-1 can ameliorate some of the effects of space flight but that space flight can also impact the normal response to IGF-1. Grant Numbers: NAGW-1197, NAGW-2328.

Animals↗
PubMed2003

Immune functions encoded by the natural killer gene complex.

There has been marked progress in our understanding of the role of natural killer (NK) cells in immune responses, mainly due to the identification of NK-cell receptors and their ligands. The genes encoding many NK-cell receptors are located in the NK-gene complex (NKC). Here, we review the properties of NKC-encoded receptors, and provide a genomic and conceptual framework for an insight into NK-cell function and biology.

Amino Acid Sequence↗
PubMed1994

The pathophysiology of biliary obstruction and its effect on phagocytic and immune function.

These studies have direct clinical relevance to the multisystem deficits seen in mechanical biliary obstruction (Fig. 3). Defects in two crucial elements of effective phagocytosis (chemotaxis and intracellular killing) have been demonstrated in obstructive jaundice. At the same time, complete diversion of bile (containing bile salts and s-IgA) from the gut lumen causes changes in the endogenous bacterial flora, loss of mucosal integrity, and decreased endotoxin inactivation, resulting in portal bacteremia, endotoxemia, and increased translocation to mesenteric lymph nodes. This increased load comes at a time when the liver is metabolically impaired and RES function is abnormal. Decreased hepatic clearance of intrabiliary bacteria may contribute to the development of cholangitis (by both ascending and hematogenous routes). Inadequate RES control of portal bacteremia results in "spillover" with subsequent systemic bacteremia and localization of organisms in the lungs where they may contribute to pulmonary dysfunction or pneumonia. Although reversal of jaundice is readily accomplished by either external or internal biliary drainage, chronic biliary obstruction results in functional alterations in the liver which are reversed, generally incompletely, only after weeks or months of decompression. External biliary decompression fails to restore the enterohepatic circulation, preventing bile salts, s-IgA, and other substances from entering the lumen of the gut. It is not as effective as internal biliary drainage in reversing RES dysfunction or restoring immune parameters. Even with internal drainage, restoration of normal function in these systems takes weeks or months. Muramyl dipeptide analogues show some promise. A possible unifying mechanism may provide the clues to further experiments which will suggest better ways of reducing the morbidity and mortality in these patients. All macrophages share common functions which include not only phagocytosis but also antigen processing and the production of cytokines. The immune dysfunction noted in obstructive jaundice may be due to inadequate or inappropriate antigen processing or cytokine production by macrophages or to abnormal hepatocyte-Kupffer cell interactions. Kupffer cells are the largest pool of macrophages. Most numerous in periportal areas, Kupffer cells process significant quantities of enteric-derived antigens and Kupffer cell blockade results in an exaggerated response to these antigens. Kupffer cells also act as important scavengers of endotoxin, which stimulates the release of TNF and IL-6.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

LFA-1 as a key regulator of immune function: approaches toward the development of LFA-1-based therapeutics.

Over the past decade, Lymphocyte Function-Associated Antigen-1 (LFA-1, alphaLbeta2, CD11a/CD18) has emerged as an attractive therapeutic target for the treatment of multiple inflammatory diseases. Its established role in the trafficking and activation of leukocytes coupled with the recent elucidation of the global conformational changes that govern its function continue to drive pharmaceutical interest in this target. This sustained interest has led to the implementation of numerous drug discovery strategies leading to the development of antibodies, peptidomimetics, and small molecules that block LFA-1 function. The most successful demonstration of clinical efficacy to date has been with Raptiva, a humanized anti-LFA-1 antibody. In clinical trials of patients with moderate to severe psoriasis, improvements in several disease specific parameters including the Psoriasis Area and Severity Index (PASI) were observed. This review article will provide an overview of LFA-1 biology and structural regulation, as well as strategies that have been adopted in pursuit of effective therapies. Recent findings with different classes of small molecule antagonists will be highlighted with an emphasis on how their different mechanisms of action on the inserted domain (I domain) of CD11a have impacted our understanding of LFA-1 function and illuminated other potential avenues for therapeutic intervention.

Animals↗