The University of Massachusetts Amherst
 
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Samuel J. Black

Professor

We are defining mechanisms of pathology in infectious (Animal African Trypanosomiasis; AAT) and non-infectious (equine laminitis) disease. AAT is caused by tsetse transmitted protozoa, is endemic in the humid and semi-humid zones of Africa, and is typically fatal in livestock, thus preventing integrated agriculture in vast regions of sub-Saharan Africa. Laminitis is a crippling disease of horses that results from failure of the digital laminae which is a two layer tissue that attaches the distal phalanx to the inner wall of the hoof capsule and hence suspends the horse’s axial skeleton in the hoof capsule. About 14% of horses develop laminitis during their life.

Current Research
Trypanosomiasis – Our studies show that African trypanosomes abnormally activate host natural killer cells causing them to delete lymphocytes and thus inhibit the development of effective protective immune responses. When this reaction is prevented by removal of the natural killer cells, the infected host effectively controls the disease. We are now dissecting the process through which the immunosuppressive natural killer cells are induced with a view of enhancing the resistance of livestock to trypanosomiasis.

Laminitis – In laminitis, the digital laminae separate at their epidermal and dermal junction. Our studies show that this results from suppression of the canonical Wnt signaling pathway in cells that line the junction, which reduces expression of proteins required to attach the cells to each other and to abutting extracellular matrix. We are now developing strategies to restore canonical Wnt signaling in the laminae which is expected to reduce or reverse laminitis.

Learn more at www.vasci.umass.edu/research-faculty/samuel-j-black

Academic Background

  • PhD University of Edinburgh
  • Postdoctoral Training: Cologne University, Germany, Stanford University, USA International Laboratory for Research in Animal Diseases, Kenya
Bockstal V, Guirnalda P, Caljon G, Goenka R, Telfer JC, Frenkel D, Radwanska M, Magez S, Black SJ. 2011. T. brucei infection reduces B lymphopoiesis in bone marrow and truncates compensatory splenic lymphopoiesis through transitional B-cell apoptosis. PLoS pathogens. 7(6):e1002089.
Black SJ, Guirnalda P, Frenkel D, Haynes C, Bockstal V. 2010. Induction and regulation of Trypanosoma brucei VSG-specific antibody responses. Parasitology. 137(14):2041-9.
Wang L, Pawlak E, Johnson PJ, Belknap JK, Eades S, Stack S, Cousin H, Black SJ. 2013 Impact of laminitis on the canonical Wnt Signaling pathway in basal epithelial cells of the equine digital laminae. PLOS One, 2013;8(2):e56025. doi: 10.1371/journal.pone.0056025. Epub 2013 Feb 6.
Trypanosoma brucei Co-opts NK Cells to Kill Splenic B2 B Cells Deborah Frenkel, Fengqiu Zhang, Patrick Guirnalda, Carole Haynes, Viki Bockstal, Magdalena Radwanska, Stefan Magez, Samuel J. Black PLos Pathogens 2016 12(7): e1005733
 
Contact Info

Department of Veterinary and Animal Sciences
427G Integrated Science Building
661 North Pleasant Street
Amherst, MA 01003-9292

(413) 545-2573
sblack@vasci.umass.edu

www.vasci.umass.edu/research-faculty/samuel-j-black