Tachykinin-mediated modulation of the immune response.
Tachykinins represent a family of peptides which have significant effects on such diverse physiological responses as gut peristalsis, vascular permeability, and the transmission of pain. Traditionally, neurons have been identified as the major source of tachykinin peptides in peripheral tissues and in the central nervous system, resulting in their classification as neuropeptides or, more specifically, as neurokinins. The fact that a variety of cell types can express one or more members of the family of neurokinin receptors accounts for the remarkable ability of these tachykinin peptides to affect multiple organ systems and numerous biological responses. Perhaps one of the most surprising findings during the last 15 years has been the understanding that expression of neurokinin receptors on leukocyte populations can be constitutive or inducible. This fact establishes a receptor-mediated mechanism by which tachykinin peptides can affect both innate and specific immune responses. Due to the numerous cytokines, chemokines, and other soluble mediators that can modulate leukocyte responses, the importance of tachykinin-mediated modulation of the immune response has met with some skepticism. The following reviews make a strong case for neurokinin receptor expression by leukocytes as a significant participant in host response. From hematopoiesis to antigen-specific T lymphocyte responses, tachykinins are present and can dramatically modulate maturation and responsiveness of these immune cells. Studies which document this surprising role for neurokinin receptor expression by leukocytes are detailed in the following reviews.
Bost
Kenneth L
KL
Department of Biology, University of North Carolina at Charlotte, Charlotte, NC 28223, USA. kbost@email.uncc.edu
D000818:Animals; D000998:Antiviral Agents / Q000378:metabolism; D001853:Bone Marrow / Q000378:metabolism; D006412:Hematopoietic Stem Cells / Q000378:metabolism; D006801:Humans; D007107:Immune System / Q000187:drug effects* / Q000473:pathology*; D007239:Infections; D007249:Inflammation; D015288:Neurokinin A / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D018040:Receptors, Neurokinin-1 / Q000378:metabolism; D013373:Substance P / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism; D015320:Tachykinins / Q000378:metabolism*
D000998:Antiviral Agents; D018040:Receptors, Neurokinin-1; D015320:Tachykinins; D013373:Substance P; D015288:Neurokinin A