Matyas Sandor

Credentials: PhD

Position title: Professor


Phone: (608) 265-8715

Room 1766 WIMR
Department of Pathology & Lab Medicine
1111 Highland Avenue
Madison, WI 53705

Sandor Lab

Focus Groups



PhD, L. Eotvos University of Sciences

Research Summary

Immune responses to infectious disease

Research Detail

  1. Develop novel treatments for controlling latent mycobacterial infections: Tuberculosis is a persistent disease effecting one third of the world’s population. My laboratory developed an innovative acute and novel latency models for in which the role of granulomas in controlling the persistence and reactivation of mycobacterial infection can be studied. We made key discoveries to understand the intriguing relationship between the environment of the host and the pathogen that regulates persistence and reactivation of mycobacteria. My goal is to develop novel cures for controlling latent mycobacterial infections. I have been supported by the Gates Foundation and the NIH to conduct these studies.
  2. To understand the protective and pathologic role of T cells in chronic infections The research in my lab focuses on how elements of the immune response help or harm the host during chronic infection. Chronic inflammation is part of the pathology of many infectious, autoimmune, and neoplastic diseases. Activated T cells are present in most chronic lesions and their cytokine production defines the character and outcome of local inflammatory reactions. Depending upon the disease, disease clearance can be facilitated by either blockage or enhancement of local T cells. My laboratory’s model of chronic inflammation is the infection-induced granulomatous reaction. This localized inflammatory response is important for controlling the growth and dissemination of infectious agents (i.e. intracellular bacteria, parasites and fungi), but the reaction is also part of the disease pathology. Using gene and protein arrays we identified and characterize molecules that regulate acute-chronic granuloma. The dynamic formation and maintenance of granulomatous lesion requires continuous cellular and bacterial traffic into and from these lesions. Supported by an NIH grant we have developed methods to study cell traffic in granulomas using cell type and bacteria specific fluorescent color codes and quantitative PCR for the different fluorescent proteins.

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