Interdisciplinary Life Science - PULSe Great research is a matter of choice

Matthew Olson

Matthew Olson Profile Picture

Assistant Professor


Contact Info:

olson126@purdue.edu
(765) 494-1254
Office: HANS 309


Training Group(s):
Immunology and Infectious Diseases


Current Research Interests:

The immune system is comprised of a variety of cell types that work in a highly organized fashion to protect the body from infection and minimize tumor formation.  This organizational process is largely carried out by the adaptive immune system with CD4+ T helper (Th) cells acting to trigger inflammation during infection and also suppress unwanted immune responses to non-harmful stimuli (i.e. allergens, food or normal body microflora).  The dual nature (i.e. activator and suppressor) of Th cells is possible due to their unique ability to sense the environment and change their function based on these environmental cues. 

Autoimmune disease occurs when the balance between the inflammatory and regulatory functions of Th cells is disrupted, resulting in excess inflammation that alters physiological processes.  Inflammatory bowel disease (IBD) and graft-versus-host disease (GVHD) are two forms of intestinal autoimmune disease and are characterized by the accumulation of highly reactive inflammatory T cells in the intestines. However, the exact mechanisms by which inflammatory Th cells arise during inflammation and cause disease are unclear. 

In the Olson lab, our goal is to better understand how CD4+ T helper cells drive intestinal inflammation by addressing these key questions:

  1. What signals drive the generation of pathogenic/inflammatory Th cells in the intestines? 
  2. How do pathogenic/inflammatory T helper cells contribute to disease?
  3. Can we therapeutically target factors that drive the generation of pathogenic T helper cells or their functional byproducts to eliminate or reduce disease?

My laboratory uses a combination of cell and molecular biology approaches to examine signaling pathways associated with T helper cell differentiation. We also utilize pre-clinical models of disease, and high throughput culturing and RNA/protein profiling techniques to identify disease mechanisms and novel mediators of inflammation.



Selected Publications:

Development of CD8 T cell immunity:

a. Olson, M.R*, McDermott, D.S.*, and Varga, S.M. The initial draining lymph node primes the bulk of the CD8 T cell response and influences memory T cell trafficking after a systemic viral infection. 2012. PLoS Pathog  8(12):e1003054. PMCID PMC3516554. * These authors contributed equally to this work.

b. Chua, B.Y.*, Olson, M.R.*, Bedoui, S., Sekiya, T., Wong, C.Y., Turner, S.J., and D.C. Jackson. 2014. The use of a TLR2 agonist-based adjuvant for enhancing effector and memory CD8 T-cell responses. Immunol Cell Biol 92(4):377-83. PMID 24394993. * These authors contributed equally to this work.

c. Russ BE, Olshanksy M, Smallwood HS, Li J, Denton AE, Prier JE, Stock AT, Croom HA, Cullen JG, Nguyen ML, Rowe S, Olson MR, Finkelstein DB, Kelso A, Thomas PG, Speed TP, Rao S, and Turner SJ. (2014) Distinct epigenetic signatures delineate transcriptional programs during virus-specific CD8(+) T cell differentiation. Immunity 41:853-865. PMCID PMC4479393.

d. Prakash, M.D., Munoz, M.A., Jain, R., Tong, P.L., Koskinen, A., Regner, A., Kleifeld, O., Ho, B., Olson, M., Turner, S.J., Mrass, P., Weninger, W., and P.I. Bird. 2014. Granzyme B promotes cytotoxic lymphocyte transmigration via basement membrane remodeling. Immunity 41:960-972. PMID 25526309.

Anti-viral T helper cell responses:

a. Olson, M.R., Seah, S.G., Edenborough, K, Doherty, P.C., Lew, A.M., and S.J. Turner.  2014. CD154+ CD4+ T-cell dependence for effective memory influenza virus-specific CD8+ T-cell responses. Immunol Cell Biol 92(7):605-11. PMID 24777309.

b. Olson, M.R., Seah SG, Cullen J, Greyer M, Edenborough K, Doherty PC, Bedoui S, Lew AM, and Turner SJ. (2014) Helping themselves: optimal virus-specific CD4 T cell responses require help via CD4 T cell licensing of dendritic cells. J Immunol 193:5420-5433. PMID 25339661.

c. Bird N.L. *, Olson, M. R. *, Hurt, A.C., Oshansky, C.M., Oh, D.Y., Reading, P.C., Sun, Y., Tang, L., Handel A., Turner, S.J., Thomas, P.G., and Katherine Kedzierska. 2015. Oseltamivir prophylaxis reduces inflammation and facilitates the establishment of cross-strain protective T cell memory to influenza viruses. PLoS One 10: e0129768. PMCID PMC4473273. *These authors contributed equally to this work.

d. Olson, M.R., Chua, B.Y., Good-Jacobson, K.L., Doherty, P.C., Jackson, D.C. and S.J. Turner. 2016. Competition within the virus-specific CD4 T cell pool limits the T follicular helper response after influenza infection. Immunol Cell Biol 94:729-40. PMID 27101922.

T helper cell differentiation:

a. Kaplan, M.H., Hufford, M.M., and M. R. Olson. 2015. The Development and in vivo function of Th9 cells. Nature Reviews Immunology 15:295-307. PMCID PMC4445728.

b. Olson, M.R., Verdan, F.F., Hufford, M.M., Dent, A.L., and M.H. Kaplan. 2016. STAT3 impairs STAT5 activation in the development of IL-9-secreting T cells. J Immunol 196:3297-304. PMCID PMC4821742.

c. Ulrich, B.J., Verdan, F.F., McKenzie, A.N., Kaplan, M.H., and M. R. Olson. 2017. STAT3 activation impairs the stability of Th9 cells. J Immunol 198(6):2302-309. PMCID PMC5340611.

d. Olson, M.R., Ulrich, B.J., Hummel, S.A., Khan, I., Meuris, B., Cherukuri, Y., Dent, A.L., Janga, S.C., and M.H. Kaplan. Paracrine IL-2 is required for optimal type 2 effector cytokine production. J Immunol In press. NIHMSID 866989.

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