Nicholas
W. Lukacs
Graduate student
Adviser: Dov Boros
Degree: Ph.D., 1992
Title of thesis: Evaluation of T cell
and granuloma responses to fractionated
soluble egg antigens in murine schistosomiasis
Contact information (as of 2/1/04):
Associate Professor
Department of Pathology
University of Michigan Medical School
5214 Medical Science I
1301 Catherine Road
Ann Arbor, MI 48109-0602
Ph: (734) 936-1874
Fax:
(734) 936-2756
Link
to Nick at U of M Work
email: nlukacs@med.umich.edu
Home
email: NA
Current activity: Nick completed Postdoctoral training in the
Department of Pathology at the University of Michigan Medical School
in the laboratory of Steven L. Kunkel, Ph.D. in 1993. Upon completion
of his Postdoctoral training he accepted a faculty position in the Department
of Pathology faculty as an Assistant Research Professor. In 2001, Nick
was promoted to the rank of Associate Professor. In addition to establishing
an independent research program, Nick has become a key member of the
Department's teaching programs and plays a significant role in the Pathology
Graduate Program.
Over the past several years the Lukacs' laboratory research has focused
on the interrelationship of cytokines, chemokines, and leukocyte activation
during asthmatic airway and Th1/Th2 cytokine immune responses. The development
of a clinically relevant mouse cockroach allergen model that demonstrates
a number of in vivo correlates to human asthma has been successfully
utilized to further elucidate novel mechanisms of pulmonary inflammation.
The areas that have been successfully investigated using the allergic
airway models include mast cell biology, eosinophilic inflammation,
and T lymphocyte activation. In addition, the laboratory has examined
the role of pulmonary viral infections (Respiratory Syncitial Virus
and Influenza) on exacerbation and increased development of allergic
asthmatic responses. Using these different models, particular leukocyte
populations that have an effect during different stages of asthmatic-like
responses within the lung have been identified. Identification of specific
cytokine and chemokine mediators that are involved in each of these
models have been elucidated and studies have correlated these pathways
to clinical disease using physiological measurements in the lung. These
studies have not only identify relevant targets for each of the individual
models, but have also helped to identify the factors involved in the
development of severe asthmatic disease.
