Serological, biochemical, and functional identity of B cell-stimulatory factor 1 and B cell differentiation factor for IgG1.

Vitetta, Ellen S.; Ohara, Junichi; Myers, Christopher D.; Layton, Judith E.; Krammer, Peter H.; Paul, William E.

doi:10.1084/jem.162.5.1726

Cited by 379 publications

(155 citation statements)

References 17 publications

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“…This result is in agreement with previous findings that IL-4 inhibits the secretion of IgG2b and IgG3 and the production of c2b and c3 germline transcripts [16][17][18][19][20][21][22][23][24][25]. IL-4 was also found to inhibit the division-linked rate of switching to IgA.…”

Section: Discussionsupporting

confidence: 82%

Decision criteria for resolving isotype switching conflicts by B cells

2005

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Isotype switching by B cells is highly regulated by a group of cytokines including IL-4, IFN-c and TGF-b. A B cell can only express one isotype at a time; however, during an immune response it may be exposed to combinations of stimuli that provide it with conflicting switching instructions. To determine how such cytokine-induced isotype switch conflicts would be resolved, the responses of B cells exposed to multiple cytokines were investigated. To eliminate complications arising from simultaneous effects of switching cytokines on proliferation, division number was used as a reference framework to monitor switching rate. The results show a clear hierarchy in which IFN-c is dominant over IL-4, and both IL-4 and IFN-c are dominant over TGF-b. These studies reveal how B cells possess a set of logical decision criteria for dealing with pathogens that invoke a range of different stimuli.

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Section: Discussionsupporting

confidence: 82%

Decision criteria for resolving isotype switching conflicts by B cells

2005

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“…Subsequent to biochemical purification (27) and molecular cloning (28,29), it was reported that II.,-4 and IgG1 enhancing factor, also called B cell differentiation factor-,/ (BCDF-~,), arc the same lymphokine (30). IL-4 was later shown to act also on T cells as well as on other cell types including monocytes, endothelial cells, and fibroblasts (13,31).…”

Section: Vol 40 No 6 1996mentioning

confidence: 99%

Interleukin‐4 stimulates rheumatoid synovial fibroblasts to express matrix metalloproteinase‐1 (tissue collagenase) and histamine H1 receptor mRNA

et al. 1996

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SUMMARY : In the present study, we investigated the effect of interleukin-4 (IL-4) on metalloproteinase 1 (MMP-1/tissue collagenase) production in human rheumatoid synovial fibroblasts. Northern blot analysis revealed that addition of IL-4 with or without histamine stimulated the cells to increase the amount of proMMP-1 mRNA, and the IL-4 with histamine addition resulted in a 3.3-fold increase compared with histamine only. Furthermore, IL-4 itself stimulated the expression of histamine H1 receptor mRNA. These results suggest that 11+-4 may play an important role in joint destruction in RA.

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“…IL-4 has biological effects on many immune cells, including B and T lymphocytes, mast cells, and macrophages, and plays a central role in regulating inflammatory and cell-mediated immune responses (Nelms et al, 1999). IL-4 acts not only as a major determinant for Th2 cell differentiation, but it also controls the specificity of immunoglobulin B cells switching to the expression of IgE and IgG (Vitetta et al, 1985;Coffman et al, 1986;Gascan et al, 1991). In addition to the effect of immune cells, IL-4 has a variety of other functions including effects in hematopoietic tissues, tissue adhesion, and inflammation (Nelms et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Interleukin-4 enhances prostate-specific antigen expression by activation of the androgen receptor and Akt pathway

et al. 2003

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Androgen receptor (AR) plays an important role in the development and progression of prostate cancer upon the action of androgen through the binding of the androgenresponsive elements (AREs) on the target genes. Abnormal activation of the AR by nonandrogen has been implicated in the progression of androgen-independent prostate cancer. The levels of interleukin-4 (IL-4) are significantly elevated in sera of patients with hormone refractory prostate cancer. The potential role of IL-4 on the activation of AR was investigated in prostate cancer cells. IL-4 enhances AR-mediated prostate-specific antigen (PSA) expression and ARE-containing gene activity through activation of the AR in the androgen ablation condition in human prostate cancer cells. The AR can also be sensitized by IL-4 and activated by significantly lower levels of androgen (10 pm of R1881) in prostate cancer cells. IL-4 enhances nuclear translocation of AR and increases binding of the AR to the ARE in LNCaP prostate cancer cells. Blocking of the Akt pathway by an Akt-specific inhibitor LY294002 abrogates IL-4-induced PSA expression and AR signaling. These results demonstrate that IL-4 enhances PSA expression through activation of the AR and Akt signaling pathways in LNCaP prostate cancer cells. Understanding IL-4-induced signaling leading to abnormal activation of AR will provide insights into the molecular mechanisms of androgen-independent progression of prostate cancer cells.

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Serological, biochemical, and functional identity of B cell-stimulatory factor 1 and B cell differentiation factor for IgG1.

Cited by 379 publications

References 17 publications

Decision criteria for resolving isotype switching conflicts by B cells

Decision criteria for resolving isotype switching conflicts by B cells

Interleukin‐4 stimulates rheumatoid synovial fibroblasts to express matrix metalloproteinase‐1 (tissue collagenase) and histamine H1 receptor mRNA

Interleukin-4 enhances prostate-specific antigen expression by activation of the androgen receptor and Akt pathway

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