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Rheumatoid synovial CD4+ T cells exhibit a reduced capacity to differentiate into IL-4-producing T-helper-2 effector cells.

Davis LS, Cush JJ, Schulze-Koops H, Lipsky PE - Arthritis Res. (2000)

Bottom Line: RAPB Tm contained significantly more IFN-gamma producers than normal cells.Normal and RAPB Tm differentiated into both IFN-gamma- and IL-4-producing effectors.RA synovial fluid (RASF) Tm demonstrated defective responsiveness, exhibiting diminished differentiation of IL-4 effectors, whereas RA synovial tissue (RAST) Tm exhibited defective generation of IFN-gamma and IL-4 producers.

View Article: PubMed Central - HTML - PubMed

Affiliation: The Harold C Simmons Arthritis Research Center and Rheumatic Diseases Division, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-8884, USA. laurie.davis@UTSouthwestern.edu

ABSTRACT
CD4+ memory T cells (Tm) from rheumatoid arthritis peripheral blood (RAPB) or peripheral blood from normal donors produced IL-2, whereas fewer cells secreted IFN-gamma or IL-4 after a brief stimulation. RAPB Tm contained significantly more IFN-gamma producers than normal cells. Many rheumatoid arthritis (RA) synovial Tm produced IFN-gamma alone (40%) and fewer cells produced IL-2 or IL-4. An in vitro model was employed to generate polarized T-helper (Th) effectors. Normal and RAPB Tm differentiated into both IFN-gamma- and IL-4-producing effectors. RA synovial fluid (RASF) Tm demonstrated defective responsiveness, exhibiting diminished differentiation of IL-4 effectors, whereas RA synovial tissue (RAST) Tm exhibited defective generation of IFN-gamma and IL-4 producers.

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T-cell growth in the presence of IL-4 and anti-IFN-γ antibody. T cells (0.5 × 106/sample) were cultured in the presence or absence of IL-4, anti-IFN-γ antibody, or both as described in Table 1. After priming, the cells were harvested and counted to assess cell growth, as described in Materials and methods. Similar results were obtained in at least two experiments. No significant difference (P > 0.05) was observed when the cells were cultured in the presence of IL-4 alone or in combination with anti-IFN-γ antibody.
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Figure 5: T-cell growth in the presence of IL-4 and anti-IFN-γ antibody. T cells (0.5 × 106/sample) were cultured in the presence or absence of IL-4, anti-IFN-γ antibody, or both as described in Table 1. After priming, the cells were harvested and counted to assess cell growth, as described in Materials and methods. Similar results were obtained in at least two experiments. No significant difference (P > 0.05) was observed when the cells were cultured in the presence of IL-4 alone or in combination with anti-IFN-γ antibody.

Mentions: As a control, cell growth during the priming cultures was monitored in the presence or absence of antibody to IFN-γ and IL-4. As shown in Fig. 5, synovial T-cell growth was not inhibited by the addition of anti-IFN-γ antibody or IL-4. These data suggest that RAPB Tm have the capacity to generate IL-4-producing or IFN-γ-producing effector cells, whereas memory T cells from RASF are inhibited in their capacity to become IL-4-producing effector cells. Further studies indicated that anti-CD28 mAb and cytokines enhanced synovial fluid Tm growth approximately fourfold above the initial input cell number. Synovial fluid T cells cultured in medium alone underwent a fourfold reduction in cell number, whereas cells cultured with cytokines alone increased in number by an average of twofold (data not shown). These data further support the conclusion that synovial fluid T cells were responsive to signals delivered by the combination of anti-CD28 and cytokines.


Rheumatoid synovial CD4+ T cells exhibit a reduced capacity to differentiate into IL-4-producing T-helper-2 effector cells.

Davis LS, Cush JJ, Schulze-Koops H, Lipsky PE - Arthritis Res. (2000)

T-cell growth in the presence of IL-4 and anti-IFN-γ antibody. T cells (0.5 × 106/sample) were cultured in the presence or absence of IL-4, anti-IFN-γ antibody, or both as described in Table 1. After priming, the cells were harvested and counted to assess cell growth, as described in Materials and methods. Similar results were obtained in at least two experiments. No significant difference (P > 0.05) was observed when the cells were cultured in the presence of IL-4 alone or in combination with anti-IFN-γ antibody.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC17825&req=5

Figure 5: T-cell growth in the presence of IL-4 and anti-IFN-γ antibody. T cells (0.5 × 106/sample) were cultured in the presence or absence of IL-4, anti-IFN-γ antibody, or both as described in Table 1. After priming, the cells were harvested and counted to assess cell growth, as described in Materials and methods. Similar results were obtained in at least two experiments. No significant difference (P > 0.05) was observed when the cells were cultured in the presence of IL-4 alone or in combination with anti-IFN-γ antibody.
Mentions: As a control, cell growth during the priming cultures was monitored in the presence or absence of antibody to IFN-γ and IL-4. As shown in Fig. 5, synovial T-cell growth was not inhibited by the addition of anti-IFN-γ antibody or IL-4. These data suggest that RAPB Tm have the capacity to generate IL-4-producing or IFN-γ-producing effector cells, whereas memory T cells from RASF are inhibited in their capacity to become IL-4-producing effector cells. Further studies indicated that anti-CD28 mAb and cytokines enhanced synovial fluid Tm growth approximately fourfold above the initial input cell number. Synovial fluid T cells cultured in medium alone underwent a fourfold reduction in cell number, whereas cells cultured with cytokines alone increased in number by an average of twofold (data not shown). These data further support the conclusion that synovial fluid T cells were responsive to signals delivered by the combination of anti-CD28 and cytokines.

Bottom Line: RAPB Tm contained significantly more IFN-gamma producers than normal cells.Normal and RAPB Tm differentiated into both IFN-gamma- and IL-4-producing effectors.RA synovial fluid (RASF) Tm demonstrated defective responsiveness, exhibiting diminished differentiation of IL-4 effectors, whereas RA synovial tissue (RAST) Tm exhibited defective generation of IFN-gamma and IL-4 producers.

View Article: PubMed Central - HTML - PubMed

Affiliation: The Harold C Simmons Arthritis Research Center and Rheumatic Diseases Division, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-8884, USA. laurie.davis@UTSouthwestern.edu

ABSTRACT
CD4+ memory T cells (Tm) from rheumatoid arthritis peripheral blood (RAPB) or peripheral blood from normal donors produced IL-2, whereas fewer cells secreted IFN-gamma or IL-4 after a brief stimulation. RAPB Tm contained significantly more IFN-gamma producers than normal cells. Many rheumatoid arthritis (RA) synovial Tm produced IFN-gamma alone (40%) and fewer cells produced IL-2 or IL-4. An in vitro model was employed to generate polarized T-helper (Th) effectors. Normal and RAPB Tm differentiated into both IFN-gamma- and IL-4-producing effectors. RA synovial fluid (RASF) Tm demonstrated defective responsiveness, exhibiting diminished differentiation of IL-4 effectors, whereas RA synovial tissue (RAST) Tm exhibited defective generation of IFN-gamma and IL-4 producers.

Show MeSH
Related in: MedlinePlus