scholarly journals The effects of iron deficiency and iron overload on cell-mediated immunity in the mouse

1994 ◽  
Vol 72 (6) ◽  
pp. 899-909 ◽  
Author(s):  
Felix O. Omara ◽  
Barry R. Blakley
Keyword(s):  
T Lymphocyte ◽  
Concanavalin A ◽  
Lymphocyte Proliferation ◽  
Interleukin 2 ◽  
Delayed Type Hypersensitivity ◽  
Cell Mediated Immunity ◽  
Spleen Cells ◽  
Deficient Diet ◽  
Cell Functions ◽  
T Lymphocyte Proliferation

The influence of Fe status on cell-mediated immunity was studied in weanling mice fed on Fe-deficient (7 mg Fe/kg), Fe-sufficient (120 mg Fe/kg) and high-Fe (3000 or 5000 mg Fe/kg) diets for 7 weeks. The contact sensitivity (CS) response to dinitrofluorobenzene (DNFB), the in vivo delayed-type hypersensitivity (DTH) response to sheep erythrocytes (SRBC) and the ability of primed spleen cells to transfer DTH response to naive normal mice were suppressed in mice consuming the Fe-deficient diet. High-Fe diets (3000 or 5000 mg Fe/kg) selectively suppressed the CS response to DNFB, but the DTH response to SRBC or the transfer of DTH response by primed spleen cells to naive normal mice remained normal. Spleen cell functions associated with the expression of class II major histocompatibility (MHC) surface antigens, concanavalin A-induced interleukin-2 (IL-2) secretion or the antigen-presenting cell (APC) ability to stimulate antigen-dependent proliferation of an SRBC-specific helper T-lymphocyte clone were not altered by Fe status. However, consistent with the suppressed DTH response in the Fe- deficient mice was the suppressed concanavalin A-induced T-lymphocyte blastogenesis and the interferon-γ (INF-γ) production by spleen cells from mice fed on the Fe-deficient diet. Spleen cells from mice fed on excess levels of Fe in the diet secreted less INF-γ than the control mice, although T- lymphocyte proliferation remained unaffected. Suppression of the cellular immune response associated with Fe deficiency may be related in part to impaired T-lymphocyte proliferation and INF-γ secretion rather than to deficits in IL-2 secretion or APC function.

scholarly journals Regulation of interleukin 2-driven T-lymphocyte proliferation by prolactin.

1990 ◽  
Vol 87 (16) ◽  
pp. 6460-6464 ◽  
Author(s):  
C. V. Clevenger ◽  
D. H. Russell ◽  
P. M. Appasamy ◽  
M. B. Prystowsky
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Interleukin 2 ◽  
T Lymphocyte Proliferation

Effect of serum factors on concanavalin A-induced T lymphocyte proliferation

1997 ◽  
Vol 56 ◽  
pp. 279
Author(s):  
Larisa G. Diachkova ◽  
Gennady V. Lutsenko ◽  
Alexander M. Sapozhnikov
Keyword(s):  
T Lymphocyte ◽  
Concanavalin A ◽  
Lymphocyte Proliferation ◽  
Serum Factors ◽  
T Lymphocyte Proliferation

scholarly journals The Capsule of Cryptococcus neoformans Reduces T-Lymphocyte Proliferation by Reducing Phagocytosis, Which Can Be Restored with Anticapsular Antibody

1999 ◽  
Vol 67 (9) ◽  
pp. 4620-4627 ◽  
Author(s):  
Rachel M. Syme ◽  
Tony F. Bruno ◽  
Thomas R. Kozel ◽  
Christopher H. Mody
Keyword(s):  
T Lymphocytes ◽  
Human Serum ◽  
Cryptococcus Neoformans ◽  
Host Defense ◽  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Therapeutic Potential ◽  
Cell Mediated Immunity ◽  
Critical Surface ◽  
T Lymphocyte Proliferation

ABSTRACT Cell-mediated immunity is critical for the host defense toCryptococcus neoformans, as demonstrated by numerous animal studies and the prevalence of the infection in AIDS patients. Previous studies have established that the polysaccharide capsule contributes to the virulence of C. neoformans by suppressing T-lymphocyte proliferation, which reflects the clonal expansion of T lymphocytes that is a hallmark of cell-mediated immunity. The present studies were performed to identify the major mechanism by which polysaccharide impairs lymphocyte proliferation, since capsular polysaccharide has the potential to affect the development of T-lymphocyte responses by stimulating production of interleukin-10 (IL-10), inhibiting phagocytosis, and inducing shedding of cell surface receptors. We demonstrate that polysaccharide inhibits lymphocyte proliferation predominantly by blocking uptake of C. neoformans, which is crucial for subsequent lymphocyte proliferation. In addition, we show that polysaccharide did not suppress lymphocyte proliferation via an IL-10-dependent mechanism, nor did it affect critical surface receptor interactions on the T cell or antigen-presenting cell. Having established that polysaccharide impairs phagocytosis, we performed studies to determine whether opsonization with human serum or with anticapsular antibody could reverse this effect. Impaired uptake and lymphocyte proliferation that were induced by polysaccharide can be enhanced through opsonization with monoclonal antibodies or human serum, suggesting that antipolysaccharide antibodies might enhance the host defense by restoring uptake of the organism and subsequent presentation to T lymphocytes. These studies support the therapeutic potential of stimulating cell-mediated immunity to C. neoformans with anticapsular antibody.

scholarly journals Cyclotides Suppress Human T-Lymphocyte Proliferation by an Interleukin 2-Dependent Mechanism

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e68016 ◽  
Author(s):  
Carsten Gründemann ◽  
Kathrin Thell ◽  
Karin Lengen ◽  
Manuel Garcia-Käufer ◽  
Yen-Hua Huang ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Interleukin 2 ◽  
T Lymphocyte Proliferation ◽  
Human T Lymphocyte ◽  
Dependent Mechanism

Inhibitory effect of anethole on T-lymphocyte proliferation and interleukin-2 production through down-regulation of the NF-AT and AP-1

2006 ◽  
Vol 20 (7) ◽  
pp. 1098-1105 ◽  
Author(s):  
Sung Su Yea ◽  
Haeng-Soon Jeong ◽  
Chun Yeon Choi ◽  
Kyung-Ran Park ◽  
Sangtaek Oh ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Interleukin 2 ◽  
Inhibitory Effect ◽  
Down Regulation ◽  
T Lymphocyte Proliferation
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