Profile: G. Miller Jonakait

Professor Emerita, NJIT

Department of Biological Sciences


We are interested in the interactions between the nervous and immune systems with a particular focus on the role of microglia, the primary mediator of immune function in the central nervous system. One interest is on the role of microglia during development. Appearing early in embryonic development, microglia produce particular growth factors that we think can have a profound influence on normal brain development. Our second interest is on the role of microglia as antigen-presenting cells (APCs). While capable of antigen presentation, microglia appear to be prohibited from expressing that function by the presence in brain of another glial cell type, the astrocyte. We have initiated several studies to determine the mechanism by which astrocytes inhibit microglial expression of the the APC phenotype.

  • Education

    A.B. in English Literature, Wellesley College, 1968.
    M.A. in English Literature, University of Chicago, 1969.
    Ph.D. in Neuroscience, Cornell University Medical College, 1978.

  • Publications

    Acevedo, G., Padala, N.K., Ni, L., and G.M. Jonakait.  (2013).  Astrocytes inhibit microglial surface expression of dendritic cell-related co-stimulatory molecules through a contact-mediated process.  J. Neurochem. 125: 575-587.

    Jonakait, G.M., Pratt, L., Acevedo, G., and L. Ni.  (2012).  Microglial regulation of cholinergic differentiation in the basal forebrain.  Dev. Neurobiol. 72: 857-864.

    Choi, K., Ni, L., and G.M. Jonakait, (2011). Fas ligation and tumor necrosis factor α activation of murine astrocytes promote heat shock factor-1 activation and heat shock protein expression leading to chemokine induction and cell survival. J. Neurochem. 116:438-448.

    Jonakait, G.M. and L. Ni, (2009). Prostaglandins compromise basal forebrain cholinergic neuron differentiation and survival: Action at EP1/3 receptors results in AIF-induced death. Brain Res. 1285:30-41.

    Jonakait, G.M. (2007). The effects of maternal inflammation on neuronal development: possible mechanisms. Intl. J. Devel. Neurosci. 25, 415-425. (<LINK>

    Li Ni, G. Acevedo, B. Muralidharan, N. Padala, J. To, and G. M. Jonakait (2007). Toll-like receptor ligands and CD154 stimulate microglia to produce a factor(s) that promotes excess cholinergic differentiation in the developing rat basal forebrain: Implications for neurodevelopmental disorders. Pediatric Res. 61, 15-20.

    Su, Y., Ganea, D., Peng, X. and G. M. Jonakait (2003). Galanin down-regulates microglial tumor necrosis factor-a production by a post-transcriptional mechanism. J. Neuroimmunol. 134, 52-60.

    Kim, W.-K., D. Ganea and G. M. Jonakait (2002). Inhibition of microglial CD40 expression by pituitary adenylyl cyclase-activating polypeptide is mediated by interleukin-10. J. Neuroimmunol. 126, 16-24.

    Delgado, M., Jonakait, G.M., D. Ganea (2002). Vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating polypeptide (PACAP) inhibit chemokine production in activated microglia. Glia. 39, 148-61.

    Kim, W.-K., Kan, Y., Ganea, D., Hart, R.P., Gozes, I., Jonakait, G.M. (2000). Vasoactive intestinal peptide and pituitary adenylyl cyclase-activating polypeptide inhibit tumor necrosis factor-a production in injured spinal cord and in activated microglia via a cAMP-dependent pathway, J. Neurosci. 20, 3622-3630.

    Jonakait, G.M., Wen,Y., Wan,Y. and Ni, L. (2000). Macrophage cell-conditioned medium promotes differentiation of undifferentiated progenitors and synergizes with nerve growth factor action in the developing basal forebrain. Exp. Neurol., 161, 285-296.

    Wei, R. and G.M Jonakait. (1999). Neurotrophins and the anti-inflammatory agents interleukin-4 (IL-4), IL-10, IL-11 and transforming growth factor-b1 (TGF-b1) down-regulate T cell costimulatory molecules B7 and CD40 on cultured rat microglia. J. Neuroimmunol., 95, 8-18.