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Kitani, Patricia Massae

doi:10.11606/t.45.2012.tde-26042012-235529

Cited by 4 publications

(4 citation statements)

References 26 publications

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“…We have Im f 1 = e 1 × · · · × e l , and we easily verify, using the calculations made to find the set of independent generators of ker 1 that1 − −1 p¯ · x p n−1 −1 is multiplicatively independent with e 1 e 2 · · · e l (the evaluations can be found in [8]). This is a contradiction; therefore, we cannot assume v = −1 p t p n 2p ∈ Im 1 Example 2.…”

Section: Validity Of Hypothesis Of Theoremmentioning

confidence: 66%

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Ferraz

Kitani

2015

Communications in Algebra

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Section: Validity Of Hypothesis Of Theoremmentioning

confidence: 66%

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Ferraz

Kitani

2015

Communications in Algebra

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“…IL-6 has been classified as a faetor that mainly induces terminal differentiation of B cells and its functional properties are quite different trom those of other B-cell stimulatory factors, sueh as B-cell stimulatory faetor-I/ IL-4 and B-cell growth faetor II/IL-5 [28]. We have previously reported that rheumatoid synovial fluid contained BCDF activity, the molecular weight and functional properties of which are similar to those of IL-6 [19). Houssiau el al.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Interleukin 6‐Like B‐Cell Differentiation Factor Production in Human Adherent Synovial Cells by Recombinant Interleukin 1

et al. 1989

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Abnormal production of immunoglobulin in the joint space is frequently observed in patients with rheumatoid arthritis (RA). We have previously demonstrated that adherent synovial cells (ASC) from patients with RA are involved in B-cell differentiation by their spontaneous production of B-cell differentiation factor (BCDF). The regulation of the production of this factor, however, has not yet been described. We investigated the effects of recombinant interleukin 1 alpha and beta (rIL-1 alpha and rIL-1 beta) on the production of BCDF in ASC. Increased production of BCDF was observed with increased rIL-1 concentration. Production of BCDF was detected 3 h after exposure of ASC to rIL-1 and increased throughout a 48-h culture. This BCDF, assayed on SKW6-CL4 cells, was found to share a common active site with interleukin 6. The effect of rIL-1 was almost neutralized by anti-IL-1 antibody and the addition of polymyxin B did not diminish the effect of rIL-1, indicating that rIL-1 itself stimulates ASC in vitro. These results suggest that IL-1 may play a regulatory role in the production of BCDF in synovial tissue.

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“…IgG2b-inducing RA-SF preparations have failed to induce in viiro differeniiation of CESS BCL cells into antibody secretory cells, a property which is believed to be caused by IL-6 [27]. Other authors have also recently described a BCDF activity in the SF of patients with RA, which eould promote the production of RF in vitro [20], but this factor has not been tested on mouse splenic cells.…”

Section: Abedi-valugerdi Ei Atmentioning

confidence: 99%

Synovial Fluid from Rheumatoid Arthritis Patients Induces Polyclonal Antibody Formation in Vivo

et al. 1989

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Our previous studies demonstrated the presence of a T-cell replacing factor in the synovial fluid (SF) of patients with rheumatoid arthritis (RA) and that RA-SF can activate, selectively, the induction of IgG2b antibody secreting cells in lipopolysaccharide (LPS)-pretreated mouse spleen cell cultures. In the present study the effect of RA-SF was tested in vivo in mice. Injection of the polyclonal activator LPS induced the production of IgM and IgG3 secreting cells in normal mice. However, the addition of RA-SF led to a selective increase in the production of IgG2b with a peak response on day 5 and IgG1 plaque-forming cells (PFC) with a peak on day 7. Neither the IgG2b nor IgG1 responses were caused by specific immunity against heterologous proteins present in RA-SF, as injection of in vitro inactive RA-SF samples did not induce PFC. The effect on B cells of RA-SF was further evaluated by injection of RA-SF in combination with LPS to the Xid B-cell deficient CBA/N mice. RA-SF had identical effects in CBA/N as in normal mice. The biological implication of these findings is discussed. Our earlier results support the idea that B cells are endogenously activated in RA patients. We have speculated that this activation is caused by the B-cell differentiation factor which is present in SF. Therefore, we also tested whether RA-SF could influence antibody-forming cells in mice that spontaneously develop autoimmunity. We found that injection of RA-SF alone, in the absence of any other activating substance, induced a very marked increase of IgG producing cells in (NZW x NZB) F1 hybrid mice. From a relatively high background level the RA-SF could still induce an up to 100-fold increase in the numbers of PFC in spleens of such mice.

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Unidades de ZCpn

Cited by 4 publications

References 26 publications

Units of ℤC_pⁿ

Units of ℤC_pⁿ

Stimulation of Interleukin 6‐Like B‐Cell Differentiation Factor Production in Human Adherent Synovial Cells by Recombinant Interleukin 1

Synovial Fluid from Rheumatoid Arthritis Patients Induces Polyclonal Antibody Formation in Vivo

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Unidades de ZCpn

Cited by 4 publications

References 26 publications

Units of ℤCpn

Units of ℤCpn

Stimulation of Interleukin 6‐Like B‐Cell Differentiation Factor Production in Human Adherent Synovial Cells by Recombinant Interleukin 1

Synovial Fluid from Rheumatoid Arthritis Patients Induces Polyclonal Antibody Formation in Vivo

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Product

Resources

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