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Immunomodulation through inhibition of multiple adhesion molecules generates resistance to autoimmune diabetes in NOD mice.
J Autoimmun. 2004 Nov; 23(3):201-9.JA

Abstract

The effect of simultaneous blockade of adhesion molecules on the development of long-term resistance to type 1 diabetes was investigated in an adoptive transfer model in NOD mice. Splenocytes isolated from acutely diabetic NOD mice injected into NOD-scid mice caused diabetes at 43 +/- 5.0 days. Treatment with anti-alpha4-integrin monoclonal antibody (mAb) delayed the onset of insulitis and significantly delayed hyperglycemia to 66 +/- 5.8 days. Combination treatment with anti-alpha4-integrin and anti-LFA-1 mAbs delayed the onset of diabetes to >100 days (p<0.0001). Combination-treated mice were subjected to a second challenge with diabetogenic splenocytes after 85 days of normoglycemia. Without additional mAb treatment they developed hyperglycemia after significant delay (72 +/- 8.1 days post-reinoculation). Splenocytes from combination-treated mice transferred protection from diabetes to naive NOD-scid mice when co-transferred with diabetogenic splenocytes. The long-surviving mice showed periislet infiltration with CD62L+ cells, which were not seen in the insulitis developing in control animals. These findings suggest that adhesion molecule blockade does not prevent homing and may affect effector cell action through activation of immunoregulatory suppressor cells, leading to protection against development of diabetes.

Authors+Show Affiliations

Transplantation Immunology Research Laboratory, Division of Transplantation, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. ninova.dora@mayo.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15501391

Citation

Ninova, Dora, et al. "Immunomodulation Through Inhibition of Multiple Adhesion Molecules Generates Resistance to Autoimmune Diabetes in NOD Mice." Journal of Autoimmunity, vol. 23, no. 3, 2004, pp. 201-9.
Ninova D, Dean PG, Stegall MD. Immunomodulation through inhibition of multiple adhesion molecules generates resistance to autoimmune diabetes in NOD mice. J Autoimmun. 2004;23(3):201-9.
Ninova, D., Dean, P. G., & Stegall, M. D. (2004). Immunomodulation through inhibition of multiple adhesion molecules generates resistance to autoimmune diabetes in NOD mice. Journal of Autoimmunity, 23(3), 201-9.
Ninova D, Dean PG, Stegall MD. Immunomodulation Through Inhibition of Multiple Adhesion Molecules Generates Resistance to Autoimmune Diabetes in NOD Mice. J Autoimmun. 2004;23(3):201-9. PubMed PMID: 15501391.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immunomodulation through inhibition of multiple adhesion molecules generates resistance to autoimmune diabetes in NOD mice. AU - Ninova,Dora, AU - Dean,Patrick G, AU - Stegall,Mark D, PY - 2004/01/13/received PY - 2004/07/08/revised PY - 2004/07/28/accepted PY - 2004/10/27/pubmed PY - 2005/5/11/medline PY - 2004/10/27/entrez SP - 201 EP - 9 JF - Journal of autoimmunity JO - J Autoimmun VL - 23 IS - 3 N2 - The effect of simultaneous blockade of adhesion molecules on the development of long-term resistance to type 1 diabetes was investigated in an adoptive transfer model in NOD mice. Splenocytes isolated from acutely diabetic NOD mice injected into NOD-scid mice caused diabetes at 43 +/- 5.0 days. Treatment with anti-alpha4-integrin monoclonal antibody (mAb) delayed the onset of insulitis and significantly delayed hyperglycemia to 66 +/- 5.8 days. Combination treatment with anti-alpha4-integrin and anti-LFA-1 mAbs delayed the onset of diabetes to >100 days (p<0.0001). Combination-treated mice were subjected to a second challenge with diabetogenic splenocytes after 85 days of normoglycemia. Without additional mAb treatment they developed hyperglycemia after significant delay (72 +/- 8.1 days post-reinoculation). Splenocytes from combination-treated mice transferred protection from diabetes to naive NOD-scid mice when co-transferred with diabetogenic splenocytes. The long-surviving mice showed periislet infiltration with CD62L+ cells, which were not seen in the insulitis developing in control animals. These findings suggest that adhesion molecule blockade does not prevent homing and may affect effector cell action through activation of immunoregulatory suppressor cells, leading to protection against development of diabetes. SN - 0896-8411 UR - https://www.unboundmedicine.com/medline/citation/15501391/Immunomodulation_through_inhibition_of_multiple_adhesion_molecules_generates_resistance_to_autoimmune_diabetes_in_NOD_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0896-8411(04)00078-2 DB - PRIME DP - Unbound Medicine ER -