https://transhumanist.ru/index.php?action=history&feed=atom&title=CD180 2026-04-08T07:21:48Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=CD180&diff=5286&oldid=prev 2021-05-12T13:37:39Z

<p>Новая страница: «CD180 antigen precursor (Lymphocyte antigen 64) (Radioprotective 105 kDa protein) [LY64] [RP105] ==Publications== {{medline-entry |title=A novel B cell populati...»</p> <p><b>Новая страница</b></p><div>CD180 antigen precursor (Lymphocyte antigen 64) (Radioprotective 105 kDa protein) [LY64] [RP105]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=A novel B cell population revealed by a CD38/CD24 gating strategy: CD38(-)CD24 (-) B cells in centenarian offspring and elderly people.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23129025<br /> |abstract=The B cell arm of adaptive immunity undergoes significant modifications with age. Elderly people are characterized by impaired B cell responses reflected in a reduced ability to effectively respond against viruses and bacteria. Alterations of immunity with advancing age (immunosenescence) have been widely studied in centenarians who are considered a good example of successful aging. In recent years, attention has shifted to centenarian offspring (CO) as a model of people genetically advantaged for healthy aging and longevity. Here, we describe the preliminary characterization of a proposed new population of memory B cells, defined as CD19( )CD38(-)CD24(-), which we find at higher frequencies in the elderly but less so in CO than healthy age-matched random controls. In addition, we found a decreased expression of RP105 ([[CD180]]), a toll-like receptor-associated molecule, on these cells. [[CD180]] downregulation may potentially be a marker of immunosenescence. Moreover, we show that these CD19( )CD38(-)CD24(-) B cells produce [[TNF]] and hypothesize that their observed expansion in the elderly might contribute to the increased inflammatory status sometimes designated &quot;inflamm-aging.&quot; <br /> |mesh-terms=* ADP-ribosyl Cyclase 1<br /> * Adult<br /> * Aged<br /> * Aged, 80 and over<br /> * Aging<br /> * B-Lymphocytes<br /> * CD24 Antigen<br /> * Cytokines<br /> * Female<br /> * Humans<br /> * Immunity, Cellular<br /> * Longevity<br /> * Lymphocyte Activation<br /> * Male<br /> * Middle Aged<br /> * Parents<br /> * Reference Values<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776115<br /> }}<br /> {{medline-entry<br /> |title=Pathogenesis of lupus-like nephritis through autoimmune antibody produced by [[CD180]]-negative B lymphocytes in NZBWF1 mouse.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22387632<br /> |abstract=Toll-like receptors appear to play an important role in the pathogenesis of lupus-like nephritis in mice. In human and mouse, [[CD180]] is a homologue of [[TLR4]]. In SLE patients, the number of [[CD180]]-negative B cells in peripheral blood changes in parallel with disease activity. In the present study using NZBWF1 mice, the population of splenic [[CD180]]-negative B cells increased with progression of renal lesions and aging. These cells produced both anti-dsDNA and histone antibodies; the peripheral blood levels of anti-dsDNA antibody increased markedly with aging. B cells infiltrating into renal lesions were [[CD180]]-negative and produced anti-dsDNA antibody. Considered together, these findings indicate that [[CD180]]-negative B cells contribute significantly to development of SLE-like morbidity in NZBWF1 mice by autoantibody production.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Antigens, CD<br /> * Autoantibodies<br /> * Autoimmune Diseases<br /> * Autoimmunity<br /> * B-Lymphocytes<br /> * Cells, Cultured<br /> * Female<br /> * Humans<br /> * Kidney<br /> * Lupus Nephritis<br /> * Mice<br /> * Mice, Inbred BALB C<br /> * Mice, Inbred NZB<br /> * Spleen<br /> <br /> |full-text-url=https://sci-hub.do/10.1016/j.imlet.2012.02.012<br /> }}</div>

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