Author
![]() |
Goff, Willard |
![]() |
BASTOS, REGINALDO - Washington State University |
![]() |
BROWN, WENDY - Washington State University |
![]() |
Johnson, Wendell |
![]() |
Schneider, David |
Submitted to: Veterinary Immunology and Immunopathology
Publication Type: Review Article Publication Acceptance Date: 6/16/2010 Publication Date: 11/15/2010 Citation: Goff, W.L., Bastos, R.G., Brown, W.C., Johnson, W.C., Schneider, D.A. 2010. The bovine spleen: interactions among splenic cell populations in the innate immunologic control of hemoparasitic infections. Veterinary Immunology and Immunopathology. 138:1-14. Interpretive Summary: An animal’s ability to clear infections of blood parasites and mount both an innate and acquired immune response against them is accomplished, in large part, in the spleen. In this review article, events that occur in the spleen during these infections such as malaria in humans and babesiosis in cattle are summarized. The tick-transmitted parasite Babesia bovis that invades red blood cells of cattle is the model for most of the experimental data summarized. Events discussed include the cell populations that become activated in response to infection and their ability to work in concert to eliminate the parasites and prime the entire immune system for a specific protective response to further exposure. Technical Abstract: Over the past several years, innate immunity has been recognized as having an important role as a front-line defense mechanism and as an integral part of the adaptive immune response. Innate immunity in cattle exposed to hemoparasites is spleen-dependent and age-related. In this review, we discuss general aspects of innate immunity and the cells involved in this aspect of the response to infection. We also provide examples of specific splenic regulatory and effector mechanisms involved in the response to Babesia bovis, an important tick-borne hemoparasitic disease of cattle. Evidence for the regulatory and effector role of bovine splenic monocytes and DC both in directing a type-1 response through interaction with splenic NK cells and gamma-delta T-cells will be presented. |