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CD4+ T cells determine the ability of spleen cells from F1 hybrid mice to induce neonatal tolerance to alloantigens and autoimmunity in parental mice.
Eur J Immunol. 1995 Jun; 25(6):1760-4.EJ

Abstract

Spleen cells from F1 hybrid mice injected into newborn parental mice induce a state of cytolytic unresponsiveness to the corresponding alloantigens. However, these mice develop a transient autoimmune syndrome characterized by the production of multiple autoantibodies and glomerulonephritis. Previous reports indicated that the depletion of F1 donor T cells, shortly prior the injection into parental mice, does not interfere with any of these events. Here, we have explored whether the continuous absence of T cells in F1 mice influences the ability of their spleen cells to induce neonatal tolerance to alloantigens and the associated autoimmune manifestations. Our results revealed that spleen cells from athymic (BALB/c x C57BL/6) F1 hybrid (CB6F1) nu/nu mice or from euthymic CB6F1 mice depleted from birth of CD4+ T cells, but not of CD8+ T cells, are unable to induce neonatal tolerance to alloantigens and autoimmune manifestations. By contrast, the partial reconstitution of T cells in CB6F1 nu/nu mice, after the neonatal graft of a syngeneic thymus, restored the capacity of spleen cells from these mice to induce tolerance and autoimmunity when injected into newborn BALB/c mice. These results demonstrate that the functional defect of spleen cells from athymic CB6F1 nu/nu mice to induce neonatal tolerance to alloantigens is directly related to the long-term absence of mature CD4+ T cells. Interestingly, a new increase in the titers of anti-DNA Ab was observed when spleen cells from athymic CB6F1 nu/nu mice were injected into adult BALB/c mice that had been tolerized at birth with normal CB6F1 spleen cells. This finding indicates that B cells from CB6F1 nu/nu mice recover their capacity to interact with alloreactive Th2 cells when they are placed into mice having functional CD4+ T cells. These data indicate that the continuous absence of CD4+ T cells causes a reversible functional defect in F1 spleen cells that determines their inability to induce neonatal tolerance and autoimmunity.

Authors+Show Affiliations

S. Inmunología, Hospital Universitario Marqués de Valdecilla, Santander, Spain.No 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

7615004

Citation

González, M, et al. "CD4+ T Cells Determine the Ability of Spleen Cells From F1 Hybrid Mice to Induce Neonatal Tolerance to Alloantigens and Autoimmunity in Parental Mice." European Journal of Immunology, vol. 25, no. 6, 1995, pp. 1760-4.
González M, Schurmans S, Ramos A, et al. CD4+ T cells determine the ability of spleen cells from F1 hybrid mice to induce neonatal tolerance to alloantigens and autoimmunity in parental mice. Eur J Immunol. 1995;25(6):1760-4.
González, M., Schurmans, S., Ramos, A., Merino, R., Lambert, P. H., & Merino, J. (1995). CD4+ T cells determine the ability of spleen cells from F1 hybrid mice to induce neonatal tolerance to alloantigens and autoimmunity in parental mice. European Journal of Immunology, 25(6), 1760-4.
González M, et al. CD4+ T Cells Determine the Ability of Spleen Cells From F1 Hybrid Mice to Induce Neonatal Tolerance to Alloantigens and Autoimmunity in Parental Mice. Eur J Immunol. 1995;25(6):1760-4. PubMed PMID: 7615004.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CD4+ T cells determine the ability of spleen cells from F1 hybrid mice to induce neonatal tolerance to alloantigens and autoimmunity in parental mice. AU - González,M, AU - Schurmans,S, AU - Ramos,A, AU - Merino,R, AU - Lambert,P H, AU - Merino,J, PY - 1995/6/1/pubmed PY - 1995/6/1/medline PY - 1995/6/1/entrez SP - 1760 EP - 4 JF - European journal of immunology JO - Eur. J. Immunol. VL - 25 IS - 6 N2 - Spleen cells from F1 hybrid mice injected into newborn parental mice induce a state of cytolytic unresponsiveness to the corresponding alloantigens. However, these mice develop a transient autoimmune syndrome characterized by the production of multiple autoantibodies and glomerulonephritis. Previous reports indicated that the depletion of F1 donor T cells, shortly prior the injection into parental mice, does not interfere with any of these events. Here, we have explored whether the continuous absence of T cells in F1 mice influences the ability of their spleen cells to induce neonatal tolerance to alloantigens and the associated autoimmune manifestations. Our results revealed that spleen cells from athymic (BALB/c x C57BL/6) F1 hybrid (CB6F1) nu/nu mice or from euthymic CB6F1 mice depleted from birth of CD4+ T cells, but not of CD8+ T cells, are unable to induce neonatal tolerance to alloantigens and autoimmune manifestations. By contrast, the partial reconstitution of T cells in CB6F1 nu/nu mice, after the neonatal graft of a syngeneic thymus, restored the capacity of spleen cells from these mice to induce tolerance and autoimmunity when injected into newborn BALB/c mice. These results demonstrate that the functional defect of spleen cells from athymic CB6F1 nu/nu mice to induce neonatal tolerance to alloantigens is directly related to the long-term absence of mature CD4+ T cells. Interestingly, a new increase in the titers of anti-DNA Ab was observed when spleen cells from athymic CB6F1 nu/nu mice were injected into adult BALB/c mice that had been tolerized at birth with normal CB6F1 spleen cells. This finding indicates that B cells from CB6F1 nu/nu mice recover their capacity to interact with alloreactive Th2 cells when they are placed into mice having functional CD4+ T cells. These data indicate that the continuous absence of CD4+ T cells causes a reversible functional defect in F1 spleen cells that determines their inability to induce neonatal tolerance and autoimmunity. SN - 0014-2980 UR - https://www.unboundmedicine.com/medline/citation/7615004/CD4+_T_cells_determine_the_ability_of_spleen_cells_from_F1_hybrid_mice_to_induce_neonatal_tolerance_to_alloantigens_and_autoimmunity_in_parental_mice_ L2 - https://doi.org/10.1002/eji.1830250641 DB - PRIME DP - Unbound Medicine ER -