Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rat monoclonal antibody (mAb) (NIM-R8), insolubilized by binding to plastic plates, induced a rapid and extensive formation of dendrite processes ('spreading') in B lymphocytes activated by anti-IgM and interleukin-4 (IL-4) or anti-CD38 and IL-4. In contrast, resting B cells were unable to spread similarly on the NIM-R8-coated plates. The NIM-R8 antibody recognized a 90,000 MW surface glycoprotein (gp90) present on both B and T lymphocytes. The expression of this molecule was greatly increased after polyclonal (lipopolysaccharide, anti-IgM plus IL-4 or concanavalin A) activation. The NIM-R8 mAb with or without IL-2 or IL-4 was unable to induce proliferation of splenic lymphocytes. Following the demonstration that the NIM-R8 mAb recognizes the murine equivalent of human CD44, the induction of spreading of activated B lymphocytes was studied using a panel of mAb recognizing different epitopes of murine CD44. All of these different mAb induced similar spreading of activated B cells. The ligand-inducible spreading of activated B lymphocytes may be an important mechanism for providing an increased cell-surface area for cell-cell or cell-matrix interactions, and thus may be an important factor controlling the response of activated lymphocytes.
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PMID:CD44-stimulated dendrite formation ('spreading') in activated B cells. 903 25

We report a 70-year-old Japanese man who had splenic lymphoma with villous lymphocytes and a complex chromosomal abnormality. No monoclonal gammopathy was present. The peripheral blood film showed lymphocytes with thin and short villi arising from one or two poles of the cells. These cells were negative for tartrate-resistant acid phosphatase stain. Immunophenotyping of peripheral blood lymphocytes showed moderate to strong expression of surface membrane IgM, IgD, IgA, and lambda as well as CD19, CD20, CD21, CD24, and HLA-DR. In addition, there was weak CD5, CD22, and CD25 expression, but no CD10, CD11c, CD23, CD38, or B-ly-7 expression. All 20 metaphases obtained from peripheral blood cells cultured for 5 days with lipopolysaccharide showed an abnormal karyotype: 47, XY, +der(3) t(3; 13) (q26; q12) inv(3) (?), t(7; 14), (q21; q11), der(13) t(3; 13) (q26; q12). Our patient followed a relatively benign clinical course and splenectomy was not performed.
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PMID:[Splenic lymphoma with villous lymphocytes and complex chromosomal abnormality]. 924 32

Mouse splenic B cells can be separated based on their distinctive expression of cell surface antigens. Marginal zone (MZ) B cells are CD38high CD21high CD23low/-, while follicular (FO) B cells are CD21int CD23int and newly formed (NF) B cells are CD21dim/- CD23-. Exploiting these phenotypic distinctions, we isolated the three B cell subsets and assessed their other phenotypic differences and functional capabilities in vitro. FO B cells proliferate more than the other B cell subsets in response to either IgM or CD38 cross-linking. MZ B cells proliferate better than FO B cells when stimulated with lipopolysaccharide (LPS), sub-optimal levels of LPS and CD38 cross-linking or CD40 ligation. When NF, FO and MZ B cells were stimulated with either LPS or LPS and interleukin-4, MZ B cells secreted more IgM and IgG3 than the other two subsets. Similarly, calcium fluxes measured within MZ B cells are larger in amplitude and more sustained after B cell receptor cross-linking than those found in the other two subsets. Collectively, these results indicate that CD38high CD21high CD23low/- MZ B cells are specially suited to play a unique role in response to antigens delivered to the MZ area.
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PMID:Marginal zone B cells exhibit unique activation, proliferative and immunoglobulin secretory responses. 934 82

CBA/N (xid) mice have a point mutation in Bruton's tyrosine kinase (btk), which results in their failure to respond to T-independent type 2 (TI-2) antigens, and to several B cell mitogens [most notably anti-immunoglobulin (Ig)] in vitro. They have reduced numbers of peripheral (B2) B cells, which are regarded as being phenotypically and functionally immature. We show here that adult CBA/N mice in fact have two distinct B cell populations: some 60% of the cells are CD23+ HSAlo sIgDhi and hence resemble recirculating, follicular (RF) B cells from normal mice, except that they are sIgMhi. The remaining 40% of xid B cells are CD23- HSAhi sIgD-/lo and resemble immature transitional (TR) B cells. TR B cells from xid mice do not synthesize DNA when cultured with lipopolysaccharide (LPS), whereas those from normal mice do so. Only the RF cells from either xid or normal mice proliferate in response to ligation of CD40. In neonatal normal mice the emergence of mitogen responsiveness followed the chronological sequence LPS-->anti-CD40-->anti-Ig approximately anti-CD38. The same developmental sequence was seen with B cells from xid mice (for LPS and anti-CD40), but it occurred at a significantly slower tempo and this correlated with the later appearance of RF-type cells. TR xid B cells express very low levels of bcl-2 and we conclude that these cells resemble very immature (bone marrow) B cells, rather than normal transitional cells. We, therefore, propose that the xid mutation imposes a multistage brake on B cell differentiation in the mouse. The available data suggest that btk is required for the positive selection of B cells throughout their differentiation in the periphery. This in turn implies that low level signaling via surface Ig is needed throughout this process in order for peripheral B cells to become functionally mature.
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PMID:A re-evaluation of the effects of X-linked immunodeficiency (xid) mutation on B cell differentiation and function in the mouse. 939 95

The Ob gene product, leptin, is an adipocyte-secreted hormone that centrally regulates weight control. However, leptin receptor is expressed not only in the central nervous system, but also in other systems such as reproductive and hematopoietic tissues. Human leptin has previously been shown to enhance cytokine production by murine peritoneal macrophages. In this paper we show that human leptin stimulates proliferation in a dose-dependent manner and functionally activates human circulating monocytes in vitro, by inducing the production of cytokines such as TNF-alpha and IL-6. Proliferation was assessed both by [3H]thymidine and bromodeoxyuridine incorporation at 48 h. We also checked the leptin stimulated monocyte expression of activation markers by flow cytometry: CD25, HLA-DR, CD38, CD71, CD11b, and CD11c expression increased after 72 h. Moreover, leptin increases the expression of the early activation marker CD69 in monocytes but not in lymphocytes. The stimulation produced by leptin is comparable to that produced by endotoxin [lipopolysaccharide (LPS)]. In addition, leptin can potentiate the stimulatory effect of LPS or PMA. Furthermore, we studied cytokine production (TNF-alpha and IL-6) simultaneously by flow cytometric detection of intracellular cytokines in the activated monocytes. Leptin produced a dose-dependent increase in the number of activated monocytes producing cytokines. These data indicate that leptin is a potent stimulatory hormone on human peripheral blood monocytes and suggest that it may have a role as a proinflammatory cytokine.
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PMID:Human leptin stimulates proliferation and activation of human circulating monocytes. 1035 75

Constitutive expression of major histocompatibility complex class II molecules (MHC II) is restricted to dendritic cells, cells of the macrophage lineage and B lymphocytes. In all three lineages, peptide fragments of captured antigen are loaded into newly synthesized MHC II molecules. In B-lineage cells, MHC II synthesis is dramatically increased on encounter with antigen, by T-cell-derived signals and by microbial products. We have previously shown that immature B cells fail to hyperexpress MHC II after antigen receptor [B-cell receptor (BCR)] ligation, but are responsive to other stimuli. Expression of the costimulatory molecule, CD86, was similarly regulated. This suggested the existence of two pathways regulating expression of these important molecules. Here we present data supporting this hypothesis. We show that activity of the enzyme phosphatidylinositol 3-kinase is critical for MHC II hyperexpression and induction of CD86 in response to ligation of the BCR or CD38, but not for responses to other stimuli including interleukin-4, lipopolysaccharide and CD40 ligation.
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PMID:A differential requirement for phosphoinositide 3-kinase reveals two pathways for inducible upregulation of major histocompatibility complex class II molecules and CD86 expression by murine B lymphocytes. 1270 23

We investigated the immunomodulatory activity of polysaccharide isolated from the root of Acanthopanax koreanum (AK) at the cellular level. AK directly increased B cell proliferation and antibody production, but did not affect the expression of IL-2, IFN-gamma or IL-4 by T cells, or T cell proliferation in vitro. Since AK cannot penetrate cells due to its large molecular mass, B cell activation may be caused by the surface binding of AK to B cell-specific receptors. The role of TLR4 as an AK receptor was shown by the fact that AK activity in B cells from C3H/HeJ mice, which are known to have a defective Toll-like receptor (TLR)-4, was found to be reduced compared with that in control cells from C3H/HeN mice. AK activity was also reduced by antibodies blocking TLR2, TLR4, CD19 or CD79b, but not by an antibody blocking CD38, which suggests AK receptor profiling in B cells. Two main differences between AK and lipopolysaccharide (LPS) were observed. First, LPS activity was inhibited by antibodies to either TLR2 or TLR4, but not by antibodies to CD19, CD79b or CD38. Another was that LPS-induced B cell proliferation was inhibited by polymyxin B (PMB), a specific inhibitor of LPS, whereas AK activity was not affected. Taken together, our results demonstrate that AK directly activates B cells, but not T cells, and suggest that AK has a broader receptor profile than LPS in B cells.
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PMID:Characterization of B cell membrane receptors of polysaccharide isolated from the root of Acanthopanax koreanum. 1275 37

CD14, originally recognized as a lipopolysaccharide (LPS) receptor, has recently been implicated in the process of T-cell suppression and apoptosis. Its soluble form has been shown to bind, in vitro, to human T cells, a process that may carry a negative signal onto these cells. We recently described a novel lymphocyte population in human peripheral blood, a population that expresses an intracellular CD14-like antigen. This novel T-cell population, composed mainly of CD8 cells and of very few CD4 cells, was found to be greatly enhanced in asymptomatic, untreated human immunodeficiency virus (HIV)-positive individuals. In the present study, we further characterized this cell population and found that it differed from other CD8 subpopulations associated with HIV infection such as CD8/CD38. In addition, we followed HIV patients under conditions of highly active antiretroviral therapy (HAART) and observed two groups of patients: patients in whom the CD14-like positive-testing T cells returned to normal within 1 to 3 months, and patients in whom it did not, in spite of a significant plasma HIV-RNA viral load decrease. Thus, this new CD14-like positive-testing lymphocyte population may represent an interesting and important component of the cellular events associated with HIV infection. On the basis of its modulation following HAART, we speculate that it may be used, in the future, as a drug-monitoring cellular marker in antiretroviral treatment.
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PMID:Overexpression of a novel lymphocyte population, positive for an intracellular CD14-like antigen, in patients positive for human immunodeficiency virus type 1. 1553 3

Mature B-2 cells expressing surface IgM and IgD proliferate upon stimulation by CD38, CD40 or lipopolysaccharide (LPS) and differentiate into IgG1-producing plasma cells in the presence of cytokines. The process of class switch recombination (CSR) from IgM to other isotypes is highly regulated by cytokines and activation-induced cytidine deaminase (AID). Blimp-1 and XBP-1 play an essential role in the terminal differentiation of switched B-2 cells to Ig-producing plasma cells. IL-5 induces AID and Blimp-1 expression in CD38- and CD40-activated B-2 cells, leading to mu to gamma1 CSR at DNA level and IgG1 production. IL-4, a well-known IgG1-inducing factor, does not induce mu to gamma1 CSR in CD38-activated B-2 cells or Blimp-1, while IL-4 induces mu to gamma1 CSR, XBP-1 expression, and IgG1 production expression in CD40-activated B-2 cells. Interestingly, the addition of 8-mercaptoguanosine (8-SGuo) with IL-4 to the culture of CD38-activated B cells can induce mu to gamma1 CSR, Blimp-1 expression, and IgG1 production. Intriguingly, 8-SGuo by itself induces AID expression in CD38-activated B cells. However, it does not induce mu to gamma1 CSR. These results imply that the mode of B-cell activation for extracellular stimulation affects the outcome of cytokine stimulation with respect to the efficiency and direction of CSR, and the requirements of the transcriptional regulator and the generation of antibody-secreting cells. Furthermore, our data suggest the requirement of additional molecules in addition to AID for CSR.
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PMID:Requirement of 8-mercaptoguanosine as a costimulus for IL-4-dependent mu to gamma1 class switch recombination in CD38-activated B cells. 1614 5

CD38, an ectoenzyme and a signaling receptor, is a novel marker of human mature monocyte-derived dendritic cells (MDDCs). The working hypothesis is that CD38 is not only a marker but also contributes to functions specifically gained by MDDCs with maturation. This was tested by assessing the role(s) of CD38 after signaling with agonistic anti-CD38 monoclonal antibodies or by blocking the interactions taking place between CD38 and CD31, its counterreceptor. The results indicate the following: (1) CD38 engagement in MDDCs ensures efficient chemotaxis and transendothelial migration driven by CC chemokine ligand 21 (CCL21); (2) CD38 is laterally associated with the CCL21-specific CC chemokine receptor 7 and with CD83 and CD11b; (3) CD38 localizes in membrane lipid domains; (4) CD38 signaling contributes to support longevity of lipopolysaccharide (LPS)-matured MDDCs after growth factor withdrawal; and (5) IFN-gamma is produced by cocultured T lymphocytes, thus affecting T-helper 1 (Th1) polarization. These data suggest that the localization of CD38 in lipid rafts and its multiple interactions with signaling receptors rule innate and adaptive immune responses by tuning DC migration, survival, and Th1-polarization ability. These findings may lay out the basis to assess the functional role(s) of human CD38 in infections, autoimmune diseases, and neoplastic disorders.
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PMID:CD38 orchestrates migration, survival, and Th1 immune response of human mature dendritic cells. 1629 98


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