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Cited by 98Iron Metabolism and DisordersT-cell and B-cell ImmunologyTrace Elements in Health

Role of iron in T cell activation: Th1 clones differ from TH2 clones in their sensitivity to inhibition of DNA synthesis caused by IGG mabs against the transferrin receptor and the iron chelator deferoxamine

Thorson, John A., Smith, Kevin M., Gomez, Francisco, Naumann, Paul W., Kemp, John D.·1991·Cellular Immunology
DOI 10.1016/0008-8749(91)90336-a
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Abstract

TH1 and TH2 helper T cell clones have been studied with respect to their sensitivity to inhibition of DNA synthesis by an IgG anti-transferrin receptor antibody (ATRA), the iron chelator deferoxamine, and the combination of the two reagents. TH1 clones are very sensitive to ATRA-mediated inhibition of DNA synthesis while TH2 clones are very resistant, but both TH1 and TH2 clones show significant down-modulation of surface transferrin receptors after ATRA exposure. TH2 clones exhibit larger chelatable iron storage pools than TH1 clones, however, and even partial chelation of TH2 cell storage iron does not fully convert a TH2 clone to the ATRA sensitivity pattern of a TH1 clone. It is therefore proposed that the greater resistance of TH2 clones to ATRA mediated inhibition derives from the combined effects of larger and less labile iron storage pools. These studies provide novel evidence indicating that nonuniform iron metabolism can exist within the T cell compartment and thus raise questions as to why such differences exist and how they can be integrated into models of the T cell activation process. These studies also suggest that the cell-mediated immune response in vivo, which is known to be sensitive to iron deficiency, may be evoked by effector cells which resemble TH1 clones insofar as iron metabolism is concerned.

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  • While all lymphocyte populations appear to depend on the acquisition of TBI, TH1 cells are exquisitely sensitive to perturbations of iron homeostasis.

    “While all lymphocyte populations appear to depend on the acquisition of TBI, T H 1 cells are exquisitely sensitive to perturbations of iron homeostasis (Thorson et al., 1991).”

    From Iron in infection and immunity (2020) · cites this paper as Thorson et al., 1991

  • Inhibition of TFR affects the proliferation of T cell subtypes differently with TH1 immune responses being more sensitive to intracellular iron depletion than TH2.

    “Inhibition of TFR affects the proliferation of T cell subtypes differently with TH1 immune responses being more sensitive to intracellular iron depletion than TH2 (Thorson et al., 1991; Mencacci et al., 1997).”

    From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Thorson et al., 1991

  • Murine Th1 clones are more sensitive to iron chelation than Th2 clones.

    “Earlier work has shown that murine Th1 clones exhibit a greater degree of sensitivity to iron chelation than do Th2 clones, implicating that iron restriction might affect Th2 cells less [129].”

    From Iron in immune cell function and host defense (2021) · cites this paper as [129]

  • Iron restriction might affect Th2 cells less than Th1 cells.

    “Earlier work has shown that murine Th1 clones exhibit a greater degree of sensitivity to iron chelation than do Th2 clones, implicating that iron restriction might affect Th2 cells less [129].”

    From Iron in immune cell function and host defense (2021) · cites this paper as [129]

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Authors
Thorson, J. A., Smith, K. M., Gomez, F., Naumann, P. W., & Kemp, J. D.
Affiliations
University of Iowa (US)
Corresponding author
Kemp, John D.
ORCID
Venue
Cellular Immunology
Publisher
Elsevier BV
Published
1991-04
Volume
134
Issue
1
Pages
126-137
ISSN
0008-8749 (ISSN-L)
DOI
10.1016/0008-8749(91)90336-a
OpenAlex
W2074412682
Cited by
98
References
24
Citations by year
2026: 3 · 2025: 8 · 2024: 6 · 2023: 6 · 2022: 6 · 2021: 11 · 2020: 5 · 2019: 4 · 2017: 2 · 2015: 2 · 2014: 2 · 2012: 1
FWCI
1.53
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Cellular Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ca037252-05)
  • National Cancer Institute (CA37252)
Topics
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
Keywords
iron metabolism, T cell activation, Th1 cells, Th2 cells, transferrin receptor, deferoxamine, iron chelation, DNA synthesis inhibition, helper T cell clones, cell-mediated immunity, iron deficiency
MeSH terms
Animals, Clone Cells, Deferoxamine, T-Lymphocytes, Helper-Inducer, Iron, Lymphocyte Activation, Receptors, Transferrin, Transferrin, Down-Regulation, T-Lymphocyte Subsets, Mice, In Vitro Techniques

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