What are granulomas?

Based upon our work we have come to define granulomas as innate sequestration responses of mononuclear leukocytes i.e. macrophages that can be amplified and or modified in cellular composition by superimposed signals arising from innate and adaptive immune recognition mechanisms.

This response is phyllogenetically ancient since it occurs among invertebrates and Ilya Metchnikov's observation of this response in starfish larva in the late 19th century launched the field of cellular immunology. Click here to see his Nobel prize winning experiment and diary notes

Granulomas are likely defensive reactions as they develop in response to many infectious agents (Table 1).  However, they likely represent a suboptimal response since sometimes the sequestered agent is not incompletely destroyed and there is often collateral damage to the normal tissues with associated fibrotic reactions. Tuberculosis is the classic granulomatous disease (click here for image of M. tuberculosis granuloma) which is sometimes associated with incomplete destruction of the causative bacteria.

Immunologic investigation has revealed that granulomas are in two major classes. 1) Foreign-body or innate type i.e. those that form in an antigen independent manner and 2) Hypersensitivity-type which are T cell-mediated responses to specific antigens associated with granulomagenic agents.  Work by our laboratory and others has shown that the latter can be further subdivided into type-1 (amplified by interferon-g and tumor necrosis factor) and type-2 (associated with interleukins 4, 5 and 13). The former are generally observed with intracellular infections whereas the latter are seen in helminthic diseases such as schistosomiasis (click here for image of S. mansoni egg granuloma) and usually contain a significant component of eosinophils.

Our laboratory has developed and characterized experimental models of innate, as well as hypersensitivity-type granulomas in order to study the molecular mechanisms which govern the development and function of these lesions.

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