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Independent regulation of 55-kDa and 75-kDa tumor necrosis factor receptors during activation of human peripheral blood B lymphocytes.
Eur J Immunol. 1991 Apr; 21(4):1033-7.EJ

Abstract

We have studied the expression of two different tumor necrosis factor receptors (TNFR; 55 kDa and 75 kDa) on resting and activated human peripheral blood B lymphocytes using specific monoclonal antibodies (mAb). Flow cytometric analysis revealed that most resting B cells expressed small amounts of the 75-kDa TNFR, and that the 75-kDa TNFR was markedly up-regulated upon stimulation with anti-mu or Staphylococcus aureus Cowan strain I (SAC). In contrast, the expression of the 55-kDa TNFR was low on resting as well as on activated cells. B cell activation was accompanied by an increased binding of biotinylated TNF-alpha, and this binding could be blocked by preincubation by utr-1 (anti-75-kDa TNRF), but not the htr (anti-55-kDa TNFR) antibodies. Notably, a number of cytokines tested (interleukin 1 to 8, interferon-gamma, TNF-alpha and -beta) did not influence the expression of either the 75-kDa or the 55-kDa TNFR when given to resting B cells. Moreover, phorbol 12-myristate 13-acetate led to an early, marked down-regulation of the 75-kDa TNFR expression, followed by a later modest increase after greater than 24 h. In contrast to other cell systems where htr mAb have been found either to mimic or to inhibit TNF action, htr mAb had insignificant effects in assays for restimulation of preactivated B cells. However, utr-1 markedly inhibited the TNF-beta but only partly inhibited the TNF-alpha-induced proliferation. Taken together, our data suggest that changes in 75-kDa protein expression is responsible for the increased TNFR expression on activated vs. resting peripheral blood B cells and that this protein also may play an important functional role.

Authors+Show Affiliations

Laboratory of Immunology, Institute for Cancer Research, Oslo, Norway.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1850359

Citation

Erikstein, B K., et al. "Independent Regulation of 55-kDa and 75-kDa Tumor Necrosis Factor Receptors During Activation of Human Peripheral Blood B Lymphocytes." European Journal of Immunology, vol. 21, no. 4, 1991, pp. 1033-7.
Erikstein BK, Smeland EB, Blomhoff HK, et al. Independent regulation of 55-kDa and 75-kDa tumor necrosis factor receptors during activation of human peripheral blood B lymphocytes. Eur J Immunol. 1991;21(4):1033-7.
Erikstein, B. K., Smeland, E. B., Blomhoff, H. K., Funderud, S., Prydz, K., Lesslauer, W., & Espevik, T. (1991). Independent regulation of 55-kDa and 75-kDa tumor necrosis factor receptors during activation of human peripheral blood B lymphocytes. European Journal of Immunology, 21(4), 1033-7.
Erikstein BK, et al. Independent Regulation of 55-kDa and 75-kDa Tumor Necrosis Factor Receptors During Activation of Human Peripheral Blood B Lymphocytes. Eur J Immunol. 1991;21(4):1033-7. PubMed PMID: 1850359.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Independent regulation of 55-kDa and 75-kDa tumor necrosis factor receptors during activation of human peripheral blood B lymphocytes. AU - Erikstein,B K, AU - Smeland,E B, AU - Blomhoff,H K, AU - Funderud,S, AU - Prydz,K, AU - Lesslauer,W, AU - Espevik,T, PY - 1991/4/1/pubmed PY - 1991/4/1/medline PY - 1991/4/1/entrez SP - 1033 EP - 7 JF - European journal of immunology JO - Eur J Immunol VL - 21 IS - 4 N2 - We have studied the expression of two different tumor necrosis factor receptors (TNFR; 55 kDa and 75 kDa) on resting and activated human peripheral blood B lymphocytes using specific monoclonal antibodies (mAb). Flow cytometric analysis revealed that most resting B cells expressed small amounts of the 75-kDa TNFR, and that the 75-kDa TNFR was markedly up-regulated upon stimulation with anti-mu or Staphylococcus aureus Cowan strain I (SAC). In contrast, the expression of the 55-kDa TNFR was low on resting as well as on activated cells. B cell activation was accompanied by an increased binding of biotinylated TNF-alpha, and this binding could be blocked by preincubation by utr-1 (anti-75-kDa TNRF), but not the htr (anti-55-kDa TNFR) antibodies. Notably, a number of cytokines tested (interleukin 1 to 8, interferon-gamma, TNF-alpha and -beta) did not influence the expression of either the 75-kDa or the 55-kDa TNFR when given to resting B cells. Moreover, phorbol 12-myristate 13-acetate led to an early, marked down-regulation of the 75-kDa TNFR expression, followed by a later modest increase after greater than 24 h. In contrast to other cell systems where htr mAb have been found either to mimic or to inhibit TNF action, htr mAb had insignificant effects in assays for restimulation of preactivated B cells. However, utr-1 markedly inhibited the TNF-beta but only partly inhibited the TNF-alpha-induced proliferation. Taken together, our data suggest that changes in 75-kDa protein expression is responsible for the increased TNFR expression on activated vs. resting peripheral blood B cells and that this protein also may play an important functional role. SN - 0014-2980 UR - https://www.unboundmedicine.com/medline/citation/1850359/Independent_regulation_of_55_kDa_and_75_kDa_tumor_necrosis_factor_receptors_during_activation_of_human_peripheral_blood_B_lymphocytes_ L2 - https://doi.org/10.1002/eji.1830210426 DB - PRIME DP - Unbound Medicine ER -