Редактирование: CD180 (раздел)

==Publications==

{{medline-entry
|title=A novel B cell population revealed by a CD38/CD24 gating strategy: CD38(-)CD24 (-) B cells in centenarian offspring and elderly people.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23129025
|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 "inflamm-aging." 
|mesh-terms=* ADP-ribosyl Cyclase 1
* Adult
* Aged
* Aged, 80 and over
* Aging
* B-Lymphocytes
* CD24 Antigen
* Cytokines
* Female
* Humans
* Immunity, Cellular
* Longevity
* Lymphocyte Activation
* Male
* Middle Aged
* Parents
* Reference Values

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776115
}}
{{medline-entry
|title=Pathogenesis of lupus-like nephritis through autoimmune antibody produced by [[CD180]]-negative B lymphocytes in NZBWF1 mouse.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22387632
|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.
|mesh-terms=* Aging
* Animals
* Antigens, CD
* Autoantibodies
* Autoimmune Diseases
* Autoimmunity
* B-Lymphocytes
* Cells, Cultured
* Female
* Humans
* Kidney
* Lupus Nephritis
* Mice
* Mice, Inbred BALB C
* Mice, Inbred NZB
* Spleen

|full-text-url=https://sci-hub.do/10.1016/j.imlet.2012.02.012
}}