Abstract
Sarcoidosis and chronic beryllium disease are noninfectious lung diseases that are characterized by the presence of noncaseating granulomatous inflammation. Chronic beryllium disease is caused by occupational exposure to beryllium containing particles, whereas the etiology of sarcoidosis is not known. Genetic susceptibility for both diseases is associated with particular MHC class II alleles, and CD4+ T cells are implicated in their pathogenesis. The innate immune system plays a critical role in the initiation of pathogenic CD4+ T cell responses as well as the transition to active lung disease and disease progression. In this review, we highlight recent insights into Ag recognition in chronic beryllium disease and sarcoidosis. In addition, we discuss the current understanding of the dynamic interactions between the innate and adaptive immune systems and their impact on disease pathogenesis.
Footnotes
This work was supported by National Institutes of Health Grants HL62410, HL102245, HL136137, and HL152756, ES011810 (to A.P.F.), and HL126736 (to A.S.M.), as well as by National Institutes of Health/National Center for Advancing Translational Sciences Colorado Clinical and Translational Science Awards Grant UL1 TR002535.
Abbreviations used in this article:
- AM
- airway macrophage
- BAL
- bronchoalveolar lavage
- CBD
- chronic beryllium disease
- DAMP
- damage-associated molecular pattern
- DC
- dendritic cell
- HMBG1
- high mobility group box protein 1
- LS
- Löfgren’s syndrome
- moDC
- monocyte-derived DC
- NDPD
- NAD-dependent protein deacetylase hst4
- Tg
- transgenic
- Treg
- regulatory T cell
- Received December 8, 2021.
- Accepted February 8, 2022.
- Copyright © 2022 by The American Association of Immunologists, Inc.
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