Mycobacterium paratuberculosis CobT Activates Dendritic Cells via Engagement of Toll-like Receptor 4 Resulting in Th1 Cell Expansion

Byun, Eui Hong; Kim, Woo Sik; Kim, Jong Seok; Won, Choul Jae; Choi, Hyongjun; Kim, Hwa Jung; Cho, Sang Nae; Lee, Keehoon; Zhang, Tiejun; Hur, Gang Min; Shin, Sung Jae

doi:10.1074/jbc.m112.391060

Cited by 23 publications

(20 citation statements)

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“…Another report has also demonstrated that Rv1917c-treated DCs secrete high levels of IL-6, IL-8, and TNF-α as well as IL-10 but not IL-12 and stimulate CD4 + T cells to produce Th2 cytokines [30]. It has been reported that several MAP proteins, including MAP1981c, MAP2541c (malate dehydrogenase), MAPCobT, and MAP1305, also induce DC maturation and Th1 polarization [18,[31][32][33]. However, no reports have examined MAP proteins that induce Th2 polarization through DC maturation.…”

Section: Discussionmentioning

confidence: 98%

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Mycobacterium avium subsp. paratuberculosis MAP1889c Protein Induces Maturation of Dendritic Cells and Drives Th2-Biased Immune Responses

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Son

et al. 2020

Cells

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Section: Discussionmentioning

confidence: 98%

“…We demonstrated that MAP1889c binds TLR4 molecules in DCs. Other MAP proteins, such as MAP1305, CobT, and MAP1989c, induce DC maturation via the TLR4 signaling pathway [32,33]. MAP stimulates bovine mononuclear cells to secrete higher IL-10 production via activation of MAPK-p38 and interactions with TLR2 [11,35].…”

Section: Discussionmentioning

confidence: 99%

Mycobacterium avium subsp. paratuberculosis MAP1889c Protein Induces Maturation of Dendritic Cells and Drives Th2-Biased Immune Responses

Park

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Son

et al. 2020

Cells

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“…Ovalbumin (OVA)-specific CD8 ϩ and CD4 ϩ T cells (responders) were obtained from splenocytes of OT-1 and OT-2 mice, respectively. These T cells were stained with 1 M carboxyfluorescein diacetate succinimidyl ester (CFSE; Invitrogen, Carlsbad, CA, USA) as previously described (22). DCs treated with OVA peptide in the presence of 10 g/ml M. abscessus CFA for 24 h were cocultured with CFSE-stained CD8 ϩ and CD4 ϩ T cells at a DC/T-cell ratio of 1:10.…”

Section: Mixed Lymphocyte Reaction (Mlr)mentioning

confidence: 99%

“…Immature mouse bone marrow-derived DCs (BM-DCs) were generated as described previously (22). Briefly, whole bone marrow cells isolated from C57BL/6, Tlr2 Ϫ/Ϫ , and Tlr4 Ϫ/Ϫ mice were washed with serum-free RPMI 1640 medium.…”

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Essential Engagement of Toll-Like Receptor 2 in Initiation of Early Protective Th1 Response against Rough Variants of Mycobacterium abscessus

et al. 2015

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dAlthough Mycobacterium abscessus (M. abscessus) is becoming more prevalent in patients without overt immunodeficiency, little is known about the factors that contribute to disease susceptibility. This study was undertaken to investigate how Toll-like receptor 2 (TLR2) functionally contributes to the generation of protective immunity against M. abscessus in a morphotype-specific manner. We found that Tlr2 M ycobacterium abscessus (sensu stricto) is an emerging rapidly growing mycobacterium (RGM) that causes a wide spectrum of infections in humans, including lung, skin, soft tissue, and bone diseases (1). M. abscessus is the most drug-resistant mycobacterial pathogen, resulting in limited therapeutic options and a high rate of treatment failure (2).Interestingly, the outcomes of mycobacterial infections can range from asymptomatic clearance to severe clinical disease (3). Different pathogen-and host-specific factors have been considered in determining the outcomes of these infections. However, it is clear that the interaction between mycobacteria and the innate and adaptive immune systems plays a central role in host defense and pathogenesis (3). In fact, the recognition of mycobacterial components by innate immune cells through various pattern recognition receptors (PRRs) induces a cytokine response that can promote early control of the infection (3, 4).Toll-like receptor (TLR)-mediated immune activation occurs only in the presence of functional TLRs, and TLR variants may exhibit altered expression, function, and recognition of signaling mechanisms, thereby increasing disease susceptibility. Healthy individuals who develop nontuberculous mycobacterial (NTM) diseases, including those caused by M. abscessus, likely have specific susceptibility factors that make them vulnerable to these infections (5). Previous studies have demonstrated an association between human TLR2 polymorphisms and tuberculosis or Mycobacterium avium complex (MAC) lung disease (6-8). In addition, TLR1 is required for TLR2 signaling, and the TLR1 single nucleotide polymorphism (SNP) I602S has been found in a cystic fibrosis cell line, resulting in a lack of recognition of M. abscessus rough variants by TLR2.Furthermore, an age-associated decrease in TLR function has been identified (9). The rate of M. abscessus infection has increased, predominantly in older women (5). Thus, delineating the molecular recognition pattern of M. abscessus is important for understanding how host resistance is induced, maintained, and regulated during infection. To date, a limited number of in vivo studies have investigated the roles of innate immunity and adaptive immunity in M. abscessus infections (10-13).Based on colony morphology on solid growth medium, there are two major variants of M. abscessus: the smooth (S) and rough (R) morphotypes (12). The cell walls of the S variant of M. abscessus are enriched with glycopeptidolipids (GPLs), and this variant

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“…avium subsp. paratuberculosis encounters dendritic cells (21,29,30) and subepithelial macrophages (11) in the lamina propria after translocation across the intestinal epithelial layer. Dendritic cells may also transport M. avium subsp.…”

Section: Avium Subsp Paratuberculosis Affects the Integrity Of Thmentioning

confidence: 99%

No Holes Barred: Invasion of the Intestinal Mucosa by Mycobacterium avium subsp. paratuberculosis

Bannantine

Bermudez

2013

Infect Immun

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The infection biology of Mycobacterium avium subsp. paratuberculosis has recently crystallized, with added details surrounding intestinal invasion. The involvement of pathogen-derived effector proteins such as the major membrane protein, oxidoreductase, and fibronectin attachment proteins have been uncovered. Mutations constructed in this pathogen have also shed light on genes needed for invasion. The host cell types that are susceptible to invasion have been defined, along with their transcriptional response. Recent details have given a new appreciation for the dynamic interplay between the host and bacterium that occurs at the outset of infection. An initial look at the global expression pathways of the host has shown a circumvention of the cell communication pathway by M. avium subsp. paratuberculosis, which loosens the integrity of the tight junctions. We now know that M. avium subsp. paratuberculosis activates the epithelial layer and also actively recruits macrophages to the site of infection. These notable findings are summarized along with added mechanistic details of the early infection model. We conclude by proposing critical next steps to further elucidate the process of M. avium subsp. paratuberculosis invasion.

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Mycobacterium paratuberculosis CobT Activates Dendritic Cells via Engagement of Toll-like Receptor 4 Resulting in Th1 Cell Expansion

Cited by 23 publications

References 53 publications

Mycobacterium avium subsp. paratuberculosis MAP1889c Protein Induces Maturation of Dendritic Cells and Drives Th2-Biased Immune Responses

Mycobacterium avium subsp. paratuberculosis MAP1889c Protein Induces Maturation of Dendritic Cells and Drives Th2-Biased Immune Responses

Essential Engagement of Toll-Like Receptor 2 in Initiation of Early Protective Th1 Response against Rough Variants of Mycobacterium abscessus

No Holes Barred: Invasion of the Intestinal Mucosa by Mycobacterium avium subsp. paratuberculosis

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