Large granular lymphocytes from B-chronic lymphocytic leukemia patients inhibit normal B cell proliferation

R. T. Perri, Neil Elliot Kay

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Large granular lymphocytes (LGL) may exert regulatory influences on B cell immunoglobulin synthesis. We, therefore, investigated the influence of LGL from controls and B cell chronic lymphocytic leukemia patients (B-CLL) on control B cell proliferation to costimulation with the F(ab')2 fragment of goat antihuman μ and B cell growth factor (BCGF). Purified LGL ( > 90% by morphology) from control and B-CLL peripheral blood were added in various concentrations to purified control B cells and incubated with anti-μ and BCGF for 3 days. [3H]-thymidine uptake of B cells was then measured. There was no proliferation of control or CLL LGL alone to the costimulatory signals of the F(ab')2 fragments of goat antihuman μ chain and BCGF. Addition of control LGL to equal numbers of control B cells did not blunt control B cell responsiveness to BCGF (with control LGL 8,649 ± 298 cpm vs. control B cells alone 8,336 ± 556 cpm, mean ± SEM). When control LGL were increased to 10:1 LGL:B cell ratio, the maximal inhibition by control LGL of control B cell proliferative response to BCGF was 23%. In contrast, addition of CLL LGL at a 1:1 LGL:B cell ratio resulted in marked impairment of the control B cell proliferative response to BCGF (with CLL LGL 3,586 ± 954 cpm vs. control B cells alone 8,649 ± 298 cpm). Inhibition by CLL LGL occurred in a cell-concentration-dependent manner. No difference in CLL LGL's inhibitory effect on either resting or activated control B cell responsiveness to BCGF was noted. Inhibition of de novo protein synthesis (by cycloheximide inhibition) of CLL LGL did impair CLL LGL's inhibitory capacity for BCGF-induced B cell proliferation. A possible explanation for these findings includes the possibility that a subgroup of LGL with B cell suppressive activity may have expanded as a host response to the B cell leukemia or as part of the disordered cell regulation in B-CLL.

Original languageEnglish (US)
Pages (from-to)166-172
Number of pages7
JournalAmerican Journal of Hematology
Volume31
Issue number3
StatePublished - 1989
Externally publishedYes

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B-Cell Chronic Lymphocytic Leukemia
B-Lymphocytes
Cell Proliferation
Lymphocytes
Intercellular Signaling Peptides and Proteins
Goats
B-Cell Leukemia

ASJC Scopus subject areas

  • Hematology

Cite this

Large granular lymphocytes from B-chronic lymphocytic leukemia patients inhibit normal B cell proliferation. / Perri, R. T.; Kay, Neil Elliot.

In: American Journal of Hematology, Vol. 31, No. 3, 1989, p. 166-172.

Research output: Contribution to journalArticle

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abstract = "Large granular lymphocytes (LGL) may exert regulatory influences on B cell immunoglobulin synthesis. We, therefore, investigated the influence of LGL from controls and B cell chronic lymphocytic leukemia patients (B-CLL) on control B cell proliferation to costimulation with the F(ab')2 fragment of goat antihuman μ and B cell growth factor (BCGF). Purified LGL ( > 90{\%} by morphology) from control and B-CLL peripheral blood were added in various concentrations to purified control B cells and incubated with anti-μ and BCGF for 3 days. [3H]-thymidine uptake of B cells was then measured. There was no proliferation of control or CLL LGL alone to the costimulatory signals of the F(ab')2 fragments of goat antihuman μ chain and BCGF. Addition of control LGL to equal numbers of control B cells did not blunt control B cell responsiveness to BCGF (with control LGL 8,649 ± 298 cpm vs. control B cells alone 8,336 ± 556 cpm, mean ± SEM). When control LGL were increased to 10:1 LGL:B cell ratio, the maximal inhibition by control LGL of control B cell proliferative response to BCGF was 23{\%}. In contrast, addition of CLL LGL at a 1:1 LGL:B cell ratio resulted in marked impairment of the control B cell proliferative response to BCGF (with CLL LGL 3,586 ± 954 cpm vs. control B cells alone 8,649 ± 298 cpm). Inhibition by CLL LGL occurred in a cell-concentration-dependent manner. No difference in CLL LGL's inhibitory effect on either resting or activated control B cell responsiveness to BCGF was noted. Inhibition of de novo protein synthesis (by cycloheximide inhibition) of CLL LGL did impair CLL LGL's inhibitory capacity for BCGF-induced B cell proliferation. A possible explanation for these findings includes the possibility that a subgroup of LGL with B cell suppressive activity may have expanded as a host response to the B cell leukemia or as part of the disordered cell regulation in B-CLL.",
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