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CD180 antigen precursor (Lymphocyte antigen 64) (Radioprotective 105 kDa protein) [LY64] [RP105]


A novel B cell population revealed by a CD38/CD24 gating strategy: CD38(-)CD24 (-) B cells in centenarian offspring and elderly people.

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

Pathogenesis of lupus-like nephritis through autoimmune antibody produced by CD180-negative B lymphocytes in NZBWF1 mouse.

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