Редактирование: CD72

B-cell differentiation antigen CD72 (Lyb-2) (CD72 antigen)

==Publications==

{{medline-entry
|title=Crucial Role of Increased Arid3a at the Pre-B and Immature B Cell Stages for B1a Cell Generation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30930899
|abstract=The Lin28b Let7  axis in fetal/neonatal development plays a role in promoting [[CD5]]  B1a cell generation as a B-1 B cell developmental outcome. Here we identify the Let7 target, Arid3a, as a crucial molecular effector of the B-1 cell developmental program. Arid3a expression is increased at pro-B cell stage and markedly increased at pre-B and immature B cell stages in the fetal/neonatal liver B-1 development relative to that in the Lin28b Let7  adult bone marrow (BM) B-2 cell development. Analysis of B-lineage restricted Lin28b transgenic (Tg) mice, Arid3a knockout and Arid3a Tg mice, confirmed that increased Arid3a allows B cell generation without requiring surrogate light chain (SLC) associated pre-[[BCR]] stage, and prevents MHC class II cell expression at the pre-B and newly generated immature B cell stages, distinct from pre-[[BCR]] dependent B development with MHC class II in adult BM. Moreover, Arid3a plays a crucial role in supporting B1a cell generation. The increased Arid3a leads higher Myc and Bhlhe41, and lower Siglec-G and [[CD72]] at the pre-B and immature B cell stages than normal adult BM, to allow [[BCR]] signaling induced B1a cell generation. Arid3a-deficiency selectively blocks the development of B1a cells, while having no detectable effect on [[CD5]]  B1b, MZ B, and FO B cell generation resembling B-2 development outcome. Conversely, enforced expression of Arid3a by transgene is sufficient to promote the development of B1a cells from adult BM. Under the environment change between birth to adult, altered [[BCR]] repertoire in increased B1a cells occurred generated from adult BM. However, crossed with B1a-restricted V /D/J IgH knock-in mice allowed to confirm that SLC-unassociated B1a cell increase and CLL/lymphoma generation can occur in aged from Arid3a increased adult BM. These results confirmed that in fetal/neonatal normal mice, increased Arid3a at the pre-B cell and immature B cell stages is crucial for generating B1a cells together with the environment for self-ligand reactive [[BCR]] selection, B1a cell maintenance, and potential for development of CLL/Lymphoma in aged mice.
|mesh-terms=* Aging
* Animals
* B-Lymphocyte Subsets
* DNA-Binding Proteins
* Gene Expression Regulation, Leukemic
* Histocompatibility Antigens Class II
* Leukemia, Lymphocytic, Chronic, B-Cell
* Mice
* Mice, Knockout
* Neoplasm Proteins
* Precursor Cells, B-Lymphoid
* Receptors, Antigen, B-Cell
* Transcription Factors
|keywords=* Arid3a
* B-1 development
* B1a
* CLL/lymphoma
* Lin28b
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428705
}}
{{medline-entry
|title=Chronic resveratrol intake reverses pro-inflammatory cytokine profile and oxidative DNA damage in ageing hybrid mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20730501
|abstract=Thymic involution and shrinkage of secondary lymphoid organs are leading causes of the deterioration of the T-cell compartment with age. Inflamm-aging, a sustained inflammatory status, has been associated with chronic diseases and shortened longevity. This is the first study to investigate the effect of treating aging hybrid mice with long-term, low-dose resveratrol (RSV) in drinking water by assessing multiple immunological markers and profiles in the immune system. We found that hybrid mice exhibited marked age-related changes in the CD3 CD4 , C3 CD8 , CD4 CD25 , CD4M and CD8M surface markers. RSV reversed surface phenotypes of old mice to that of young mice by maintaining the CD4  and CD8  population in splenocytes as well as reducing CD8 CD44  (CD8M) cells in the aged. RSV also enhanced the CD4 CD25  population in old mice. Interestingly, pro-inflammatory status in young mice was transiently elevated by RSV but it consequently mitigated the age-dependent increased pro-inflammatory cytokine profile while preserving the anti-inflammatory cytokine condition in the old mice. Age-dependent increase in 8OHdG, an oxidative DNA damage marker was ameliorated by RSV. Immunological-focused microarray gene expression analysis showed that only the [[CD72]] gene was significantly downregulated in the 12-month RSV-treated mice compared to age-matched controls. Our study indicates that RSV even at low physiological relevant levels is able to affect the immune system without causing marked gene expression changes.
|mesh-terms=* Aging
* Animals
* Antigens, Surface
* Antioxidants
* Cell Count
* Cytokines
* DNA Damage
* Inflammation
* Mice
* Mice, Inbred Strains
* Models, Animal
* Oligonucleotide Array Sequence Analysis
* Oxidative Stress
* Resveratrol
* Spleen
* Stilbenes
* T-Lymphocyte Subsets

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168607
}}
{{medline-entry
|title=Chronic lung inflammation in aging mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17628550
|abstract=To determine whether aging is associated with a pro-inflammatory shift in the lung, inflammation and inflammation-related gene expression in the lungs of 12-week-old and 24-month-old Balb/c mice were studied. cDNA microarray and quantitative reverse transcription-polymerase chain reaction analyses showed that eight inflammation-related genes, including CD20, Burkitt lymphoma receptor 1, CXCR-3, provirus integration site for Moloney murine leukemia virus-2, [[CD72]], IL-8RB, C-Fgr, and CD8beta, were upregulated in the aged mice. Immunohistochemistry showed that the lungs of the aged mice contained increased numbers of [[CD4]] cells, CD8 cells, B cells and macrophages. These results suggest that a pro-inflammatory shift occurs in the lungs of mice with aging.
|mesh-terms=* Aging
* Animals
* Chronic Disease
* Female
* Gene Expression Regulation
* Mice
* Mice, Inbred BALB C
* Pneumonia

|full-text-url=https://sci-hub.do/10.1016/j.febslet.2007.06.075
}}
{{medline-entry
|title=[[CD72]] ligation regulates defective naive newborn B cell responses.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/9023424
|abstract=The biological basis for reduced Ig production by naive newborn B cells compared to adult peripheral blood B cells is not fully understood. In a Con A   IL-2 T cell-dependent system using "competent" adult T cells, adult B cells produced large amounts of IgM, IgG, and IgA, while cord B cells were restricted to low levels of only IgM production. Cord B cell activation was also diminished. The contribution of specific B-T cell contact-mediated events to the diminished cord B cell response in this system, using mAbs to [[CD40]], [[CD28]], [[CD80]], and [[CD72]], were investigated, as well as regulation of B cell Ig production by cytokines. alpha[[CD72]] ligation increased cord B cell activation and IgM production, but did not affect adult B cells. Blocking alpha[[CD40]] mAb inhibited cord B cell Ig production completely, but only partly inhibited adult B cell Ig production even at high concentration, suggesting a greater sensitivity of cord B cells to disruption of the [[CD40]]-[[CD40]]L interaction. Addition of IL-10 did not increase cord B cell Ig production, while adult B cell Ig production was increased. However, combined addition of IL-10 and alpha[[CD72]] significantly increased cord B cell Ig production over that in the presence of either alpha[[CD72]] or IL-10 alone, but had no effect on adult B cells over that of IL-10 alone. These data suggest that the diminished T cell-dependent response of cord B cells is due to reduced or absent [[CD72]] ligation. [[CD72]] ligation plays an important role in the induction of primary responses by naive B cells. [[CD72]] modulation of naive B cell sensitivity to IL-10 stimulation may have implications in the induction of class switch, which is deficient in newborn B cells. Since all T cells express [[CD5]] constitutively, these data also suggest the existence of another ligand for [[CD72]].
|mesh-terms=* Adult
* Aging
* Antibodies, Monoclonal
* Antibody Formation
* Antigens, CD
* Antigens, Differentiation, B-Lymphocyte
* B-Lymphocytes
* Cell Differentiation
* Cells, Cultured
* Concanavalin A
* Cytokines
* Fetal Blood
* Histocompatibility Antigens Class II
* Humans
* Interleukin-10
* Interleukin-2
* Lymphocyte Activation
* Lymphocyte Cooperation
* Middle Aged
* T-Lymphocytes

|full-text-url=https://sci-hub.do/10.1006/cimm.1996.1033
}}
{{medline-entry
|title=Characteristics and development of the murine B-1b (Ly-1 B sister) cell population.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/1376053
|abstract=In this paper we have outlined the evidence for two distinct branches of the B-1 cell lineage. The data show that phenotypically B-1a and B-1b cells are essentially identical, distinguished only by the presence or absence of the [[CD5]] antigen. Functionally no differences between the two populations have yet been identified. Both produce anti-PtC antibodies, a specificity not observed in conventional B cells. Both produced high levels of IgM as measured in adoptive transfer experiments. Developmentally, B-1a and B-1b cells are indistinguishable with respect to generation from progenitors present in fetal liver and omentum, feedback regulation of new B-1a and B-1b cells from bone marrow, self-replenishment from Ig  cells following adoptive transfer, and the generation of clonal populations. The major difference in the two populations is seen in the development of B-1a and B-1b cells from B220- progenitors in the adult bone marrow. Although B220- B-1a progenitors are rare in adult (greater than 6 weeks) bone marrow, the progenitors for B-1b cells persist well into adulthood. Our understanding of B-1b cell ontogeny is at a stage similar to that of B-1a cells five years ago. We have evidence from transfer experiments that strongly suggests the existence of two distinct progenitors for B-1a and B-1b, but we have yet to physically separate these progenitors as Solvansen et al. have done for B-1 and conventional B cells. Furthermore we must determine whether the B-1b cells that develop from fetal liver and bone marrow are functionally and developmentally equivalent to those that develop from adult bone marrow. As with B-1a cells, the role of B-1b cells in the immune system is unclear. Although we have not yet discerned functional differences between B-1a and B-1b, given the recent identification of [[CD72]] (Lyb-2) as the ligand for [[CD5]], it is tempting to speculate that B-1a cells are more involved in B-B cell interactions such as idiotype-anti-idiotype regulation of the early B-cell repertoire and that B-1b cells are more involved in B-T cell interactions. Whatever their function, it is clear that in trying to understand the role of the B-1 lineage it is important to consider both the B-1a and B-1b lineages.
|mesh-terms=* Aging
* Animals
* Antigens, CD
* B-Lymphocyte Subsets
* CD5 Antigens
* Embryonic and Fetal Development
* Hematopoietic Stem Cells
* Immunoglobulin M
* Immunotherapy, Adoptive
* Mice
* Mice, Inbred Strains
* Phenotype
* Spleen

|full-text-url=https://sci-hub.do/10.1111/j.1749-6632.1992.tb24591.x
}}