B7/CD28 Costimulation Is Critical in Susceptibility to<i>Pseudomonas aeruginosa</i>Corneal Infection: A Comparative Study Using Monoclonal Antibody Blockade and CD28-Deficient Mice

Hazlett, Linda D.; McClellan, Sharon A.; Barrett, Ronald P.; Rudner, Xiaowen L.

doi:10.4049/jimmunol.166.2.1292

Cited by 20 publications

(11 citation statements)

References 39 publications

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“…Earlier reports also indicate that these Langerhans cells, which are more numerous in the peripheral cornea, have a role in corneal transplantation rejection and in the host response in Herpes simplex keratitis and in Pseudomonas aeruginosa keratitis (35–38). …”

Section: Discussionmentioning

confidence: 92%

Bone Marrow Chimeras and c-fms Conditional Ablation (Mafia) Mice Reveal an Essential Role for Resident Myeloid Cells in Lipopolysaccharide/TLR4-Induced Corneal Inflammation

Chinnery

Carlson

Sun

et al. 2009

The Journal of Immunology

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The mammalian cornea contains an extensive network of resident macrophages and dendritic cells. To determine the role of these cells in LPS-induced corneal inflammation, TLR4−/− mice were sublethally irradiated and reconstituted with bone marrow cells from either enhanced GFP (eGFP)+/C57BL/6 or eGFP+/TLR4−/− mice. The corneal epithelium was abraded, LPS was added topically, and cellular infiltration to the corneal stroma and development of corneal haze were examined after 24 h. TLR4−/− mice reconstituted with C57BL/6, but not TLR4−/− bone marrow cells donor cells were found to cause infiltration of eGFP+ cells to the cornea, including neutrophils, and also increased corneal haze compared with saline-treated corneas. In a second experimental approach, corneas of transgenic macrophage Fas induced apoptosis (Mafia) mice were stimulated with LPS. These mice express eGFP and a suicide gene under control of the c-fms promoter, and systemic treatment with the FK506 dimerizer (AP20187) causes Fas-mediated apoptosis of monocytic cells. AP20187-treated mice had significantly fewer eGFP+ cells in the cornea than untreated mice. After stimulation with LPS neutrophil recruitment and development of corneal haze were impaired in AP20187-treated mice compared with untreated controls. Furthermore, LPS induced CXCL1/KC and IL-1α production within 4 h in corneas of untreated Mafia mice, which is before cellular infiltration; however, cytokine production was impaired after AP20187 treatment. Together, results from both experimental approaches demonstrate an essential role for resident corneal monocytic lineage cells (macrophages and dendritic cells) in development of corneal inflammation.

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Section: Discussionmentioning

confidence: 92%

Bone Marrow Chimeras and c-fms Conditional Ablation (Mafia) Mice Reveal an Essential Role for Resident Myeloid Cells in Lipopolysaccharide/TLR4-Induced Corneal Inflammation

Chinnery

Carlson

Sun

et al. 2009

The Journal of Immunology

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“…CD28, inducible costimulator (ICOS), and cytolytic T lymphocyte-associated antigen (CTLA) -4 are all involved in the DTH reaction [18]–[21]. NKG2D is a costimulatory receptor expressed on NK cells, CD8 + T cells, NKT cells, and γδ T cells [22]–[24].…”

Section: Introductionmentioning

confidence: 99%

NKG2D+ IFN-γ+ CD8+ T Cells Are Responsible for Palladium Allergy

et al. 2014

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Nickel, cobalt, and chromium are well known to be causal agents of allergic contact dermatitis. Palladium (Pd) can also cause allergic disease and exposure results from wide use of this metal in dental restorations and jewelry. Metal allergy is categorized as a delayed-type hypersensitivity, and metal-responsive T cell clones have been isolated from allergic patients. However, compared to nickel, little is known about the pathology of allergic disease mediated by Pd, and pathogenic T cells are poorly understood. To identify the pathogenic T cells that are responsible for onset of Pd allergy, we enriched metal-responsive lymphocytes by sequential adoptive transfer of involved lymph node cells. Here we show that sequential adoptive transfer gradually increased the incidence and the intensity of Pd allergy, and CD8+ T cells are responsible for the disease as CD8+ T cell-depleted mice and β2-microglobulin-deficient mice did not develop Pd allergy. In addition, we found that draining lymph node cells skewed toward CD8+ T cells in response to Pd challenge in 8th adoptive transferred recipient mice. The CD8+ T cells expressed NKG2D, a costimulatory molecule involved in the production of IFN-γ. NKG2D ligand was also induced in Pd-injected tissues. Furthermore, both NKG2D ligand-transgenic mice, where NKG2D is downmodulated, and IFN-γ-deficient mice showed impaired Pd allergy. Taken together, these results indicate that IFN-γ-producing NKG2D+ CD8+ T cells are responsible for Pd allergy and suggest that NKG2D is a potential therapeutic target for treatment of metal allergy.

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“…(Kwon & Hazlett, 1997) Cytokines released by CD4+ T cell and LC result in infiltration of higher numbers of PMN, eventually leading to increased corneal. (Hazlett et al, 2001;Hazlett et al, 2002) While some propose that in order to minimise this collateral damage to ocular tissues, therapies should consider directing the immune response from CD4+/Th1 mediated towards a Th2 pathway, (Kijlstra, 1994) others are of the opinion that it is the balance between pro-and anti-inflammatory mediators that is of greater significance in pseudomonal keratitis. (Hazlett, 2004) (O'Callaghan et al, 1996) …”

Section: Pseudomonas Keratitismentioning

confidence: 99%