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MIP-1alpha and MCP-1 differentially regulate acute and relapsing autoimmune encephalomyelitis as well as Th1/Th2 lymphocyte differentiation.
J Leukoc Biol. 1997 Nov; 62(5):681-7.JL

Abstract

Chemokines are a family of small-molecular-weight cytokines that induce chemotaxis and chemokinesis of leukocytes. These molecules are ligands for seven-transmembrane, G-protein-linked receptors and are known to activate integrins on the surface of leukocytes and other cells as well as induce a number of signaling events. They play a significant role in the migration of leukocytes from blood into tissue during inflammatory processes. We tested the role of chemokines in experimental autoimmune encephalomyelitis (EAE) and found that macrophage inflammatory protein-1alpha (MIP-1alpha) correlated with acute disease development, whereas monocyte chemotactic protein-1 (MCP-1) did not. In contrast, MCP-1 production in the central nervous system correlated with relapsing EAE development. Moreover, anti-MIP-1alpha, but not anti-MCP-1, inhibited development of acute but not relapsing EAE, whereas anti-MCP-1 significantly reduced the severity of relapsing EAE. To test the effects of chemokines on the differentiation of naive T cells, TCR transgenic splenic T cells (Tg+ T cells) from DO11.10 OVA TCR transgenic mice were used as a source of Th0 cells and were stimulated with specific anti-clonotypic monoclonal antibodies in the presence of MIP-1alpha, MCP-1, or controls. MIP-1alpha drove Th0 cells to differentiate to Th1, whereas MCP-1 drove Th0 cells to differentiate to Th2. Similarly, MCP-1, but not MIP-1alpha significantly inhibited the adoptive transfer of EAE when included in in vitro activation cultures, further suggesting a regulatory anti-inflammatory property. These results suggest a differential role for CC chemokines in the development and activation of T cells during autoimmune inflammatory diseases.

Authors+Show Affiliations

Department of Pathology, Robert H. Lurie Cancer Center, Northwestern University Medical School, Chicago, Illinois 60611, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9365124

Citation

Karpus, W J., and K J. Kennedy. "MIP-1alpha and MCP-1 Differentially Regulate Acute and Relapsing Autoimmune Encephalomyelitis as Well as Th1/Th2 Lymphocyte Differentiation." Journal of Leukocyte Biology, vol. 62, no. 5, 1997, pp. 681-7.
Karpus WJ, Kennedy KJ. MIP-1alpha and MCP-1 differentially regulate acute and relapsing autoimmune encephalomyelitis as well as Th1/Th2 lymphocyte differentiation. J Leukoc Biol. 1997;62(5):681-7.
Karpus, W. J., & Kennedy, K. J. (1997). MIP-1alpha and MCP-1 differentially regulate acute and relapsing autoimmune encephalomyelitis as well as Th1/Th2 lymphocyte differentiation. Journal of Leukocyte Biology, 62(5), 681-7.
Karpus WJ, Kennedy KJ. MIP-1alpha and MCP-1 Differentially Regulate Acute and Relapsing Autoimmune Encephalomyelitis as Well as Th1/Th2 Lymphocyte Differentiation. J Leukoc Biol. 1997;62(5):681-7. PubMed PMID: 9365124.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MIP-1alpha and MCP-1 differentially regulate acute and relapsing autoimmune encephalomyelitis as well as Th1/Th2 lymphocyte differentiation. AU - Karpus,W J, AU - Kennedy,K J, PY - 1997/11/19/pubmed PY - 1997/11/19/medline PY - 1997/11/19/entrez SP - 681 EP - 7 JF - Journal of leukocyte biology JO - J Leukoc Biol VL - 62 IS - 5 N2 - Chemokines are a family of small-molecular-weight cytokines that induce chemotaxis and chemokinesis of leukocytes. These molecules are ligands for seven-transmembrane, G-protein-linked receptors and are known to activate integrins on the surface of leukocytes and other cells as well as induce a number of signaling events. They play a significant role in the migration of leukocytes from blood into tissue during inflammatory processes. We tested the role of chemokines in experimental autoimmune encephalomyelitis (EAE) and found that macrophage inflammatory protein-1alpha (MIP-1alpha) correlated with acute disease development, whereas monocyte chemotactic protein-1 (MCP-1) did not. In contrast, MCP-1 production in the central nervous system correlated with relapsing EAE development. Moreover, anti-MIP-1alpha, but not anti-MCP-1, inhibited development of acute but not relapsing EAE, whereas anti-MCP-1 significantly reduced the severity of relapsing EAE. To test the effects of chemokines on the differentiation of naive T cells, TCR transgenic splenic T cells (Tg+ T cells) from DO11.10 OVA TCR transgenic mice were used as a source of Th0 cells and were stimulated with specific anti-clonotypic monoclonal antibodies in the presence of MIP-1alpha, MCP-1, or controls. MIP-1alpha drove Th0 cells to differentiate to Th1, whereas MCP-1 drove Th0 cells to differentiate to Th2. Similarly, MCP-1, but not MIP-1alpha significantly inhibited the adoptive transfer of EAE when included in in vitro activation cultures, further suggesting a regulatory anti-inflammatory property. These results suggest a differential role for CC chemokines in the development and activation of T cells during autoimmune inflammatory diseases. SN - 0741-5400 UR - https://www.unboundmedicine.com/medline/citation/9365124/MIP_1alpha_and_MCP_1_differentially_regulate_acute_and_relapsing_autoimmune_encephalomyelitis_as_well_as_Th1/Th2_lymphocyte_differentiation_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0741-5400&date=1997&volume=62&issue=5&spage=681 DB - PRIME DP - Unbound Medicine ER -