Research Interest: Innate immunity in tuberculosis
Ph.D.: Cornell University
Postdoctoral: Cornell University
Currently accepting new students.
Tuberculosis (TB), a disease caused by Mycobacterium tuberculosis (Mtb) infection, remains one of the biggest infectious disease threats and a leading cause of death worldwide. The lack of understanding of the nature of protective immunity against TB hinders the development of an effective vaccine. Macrophages are the most abundant host cells at site of Mtb infection and have been implicated in both disease control and progression. Moreover, the complexity of macrophages is reflected by their origins, heterogeneity and metabolism, all of which govern the functions of these cells in various tissues under homeostatic and inflammatory conditions. We have demonstrated that lung macrophages with distinct developmental lineages acquire unique metabolic states and exhibit differential levels of permissiveness to Mtb survival and growth at early stages of infection. These studies provided the evidence that cell-intrinsic features of differing subsets of lung macrophages dominate the host response to Mtb infection. The overall goal of my laboratory is to define the protective immunity against Mtb. We focus on the biology of lung macrophages and aim to understand the ontogeny and immunometabolism of those cells during Mtb infection. Ultimately, this knowledge will inform the development of vaccines and novel therapeutic interventions against this pathogen. Moreover, these studies may also have a broad impact on other pulmonary diseases.
- Huang L, Ye K, McGee MC, Nidetz NF, Elmore JP, Limper CB, Southard TL, Russell DG, August A, Huang W. IL-2 inducible T cell kinase (ITK) deficiency impairs early pulmonary protection against Mycobacterium tuberculosis infection. Frontiers in Immunology, 2020; 10:3103. [PMID: 32038633]
- Zhang Z, Schlamp F, Huang L, Clark H, Brayboy L. Inflammaging is associated with shifted macrophage ontogeny and polarization in mouse ovary. Reproduction, 2020; 159(3):325-337. [PMID: 31940276]
- Pisu D, Huang L, Grenier JK, Russell DG. Dual RNA-seq of Mycobacterium tuberculosis-infected macrophages in vivo reveals ontologically-distinct host-pathogen interactions. Cell Reports, 2020; 30 (2), 335-350. [PMID: 31940480]
- Russell DG, Huang L, VanderVen BC. Immunometabolism at the interface between macrophages and pathogens. Nature Reviews Immunology, 2019; 19, 291-304. [PMID: 30679807]
- Huang L, Nazarova EV, Tan S, Liu Y, Russell DG. Growth of Mycobacterium tuberculosis in vivo segregates with host macrophage metabolism and ontogeny. Journal of Experimental Medicine, 2018; 215 (4), 1135-1152. [PMID: 29500179]
- Huang L, Russell DG. Protective immunity against tuberculosis: what does it look like and how do we find it? Current Opinion in Immunology, 2017; 48, 44-50. [PMID: 28826036]
- Liu Y, Tan S, Huang L, Abramovitch RB, Rohde KH, Zimmerman MD, Chen C, Dartois V, VanderVen BC, Russell DG. Immune activation of the host cell induces drug tolerance in Mycobacterium tuberculosis both in vitro and in vivo. Journal of Experimental Medicine, 2016: 213(5):809-25. [PMID: 27114608]
- Huang L, Appleton JA. Eosinophils in helminth infection: Defenders and Dupes. Trends in Parasitology, 2016; 32 (10): 798-807. [PMID: 27262918]
- Huang L, Beiting DP, Gebreselassie NG, Gagliardo LF, Ruyechan MC, Lee NA, Lee JJ, Appleton JA. Eosinophils and IL-4 support nematode growth coincident with an innate response to tissue injury. PLOS Pathogens, 2015; Dec 31;11(12):e1005347. [PMID: 26720604]
- Huang L, Gebreselassie NG, Gagliardo LF, Ruyechan MC, Luber KL, Lee NA, Lee JJ, Appleton JA. Eosinophils are required for protective responses against secondary nematode infection. Journal of Immunology, 2015; 194(1): 283-290. [PMID: 25429065]
- Huang L, Gebreselassie NG, Gagliardo LF, Ruyechan MC, Lee NA, Lee JJ, Appleton JA. Eosinophil-derived IL-10 supports chronic nematode infection. Journal of Immunology, 2014; 193(8): 4178-87. [PMID: 25210122]