Peptides Derived From Icam-1 and Lfa-1 Modulate T Cell Adhesion and Immune Function in a Mixed Lymphocyte Culture1

Tibbetts, Scott A.; Chirathaworn, Chintana; Nakashima, Mitsuyoshi; Jois, D. S. Seetharama; Siahaan, Teruna J.; Chan, Marcia A.; Benedict, Stephen H.

doi:10.1097/00007890-199909150-00015

Cited by 44 publications

(43 citation statements)

References 35 publications

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“…T cells were isolated from fresh tonsils or peripheral blood from multiple healthy donors as previously described (20). Briefly, cell suspensions from minced tonsils or peripheral blood were layered over Ficoll-Hypaque (Pharmacia, Piscataway, NJ) and spun for 30 min at 670 ϫ g to isolate mononuclear cells.…”

Section: Cell Purification and Culturementioning

confidence: 99%

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Stimulation Through Intercellular Adhesion Molecule-1 Provides a Second Signal for T Cell Activation

Chirathaworn

Kohlmeier

Tibbetts

et al. 2002

The Journal of Immunology

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102

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Regulation of T cell activation requires two signals. First, appropriately presented Ag in the context of MHC interacts with the T cell Ag receptor-CD3 complex. The best-studied second signal is CD28, which resides on the T cell and responds to its counter receptor, B7. A second signal also can be delivered through LFA-1 residing on the T cell, responding to its counter receptor ICAM-1 residing on a different cell. Characterization of a second signal is tied to its ability to costimulate (along with stimulation through the TCR) proliferation, IL-2 secretion, and coactivation of phosphatidylinositol 3-kinase. We examined whether ICAM-1, residing on the T cell surface, could deliver a second signal into that T cell. Costimulation through CD3 plus ICAM-1 caused increased T cell proliferation, increased expression of the activation marker CD69, increased transcription through the IL-2 regulatory region, and increased secretion of selected Th1 but not Th2 cytokines. Costimulation through CD3 plus ICAM-1 caused synergistic activation of phosphatidylinositol 3-kinase. Finally, the combination of anti-CD3 plus anti-ICAM-1 (but not anti-CD3 alone) caused prolonged proliferation of naive T cells in a manner similar to costimulation through LFA-1 or CD28. Thus, we demonstrate for the first time that ICAM-1 resident on a T cell can deliver a costimulatory signal into that T cell.

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Section: Cell Purification and Culturementioning

confidence: 99%

“…Transiently transfected cells (7.5 ϫ 10 6 /well, 2 wells/sample) were stimulated on plates coated at 37°C for 2 h with 50 l of anti-CD3 (2 g/ml), anti-LFA-1 (10 g/ml), anti-CD28 (2 g/ml), or anti-ICAM-1 (10 g/ml) in PBS (20). Before the addition of cells, plates were washed three times with PBS.…”

Section: Luciferase Assaysmentioning

confidence: 99%

Stimulation Through Intercellular Adhesion Molecule-1 Provides a Second Signal for T Cell Activation

Chirathaworn

Kohlmeier

Tibbetts

et al. 2002

The Journal of Immunology

Self Cite

102

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“…4). Although anti-ICAM-1 antibody is known to inhibit T-cell adhesion and immune function (31), it seems that the anti-ICAM-1 MAb used in this study did not modify the activation of HGECs but inhibited the direct binding of C. albicans with HGECs. Our result supported a previous report that ICAM-1 plays a role in the adherence of C. albicans to pulmonary vascular endothelial cells (34).…”

Section: Increased Induction Of Interleukin 8 (Il-mentioning

confidence: 61%

Intercellular adhesion molecule 1-dependent activation of interleukin 8 expression in Candida albicans-infected human gingival epithelial cells

Egusa

Nikawa

Makihira

et al. 2005

International Congress Series

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Increased induction of interleukin 8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by oral epithelial cells may play a role in the host defense mechanism in oropharyngeal candidiasis; however, little is known about the expression feature of these molecules on human gingival epithelial cells (HGECs) during Candida albicans infection. In this report we present evidence that neutralization with antibody against ICAM-1 inhibited both the adherence of C. albicans to HGECs and the Candida-induced production of IL-8, suggesting a role for ICAM-1 in recognition and signaling in HGECs to express IL-8 upon infection with C. albicans.

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“…In this case, both ICAM-1 and MHC-II receptors were modeled as if they were protruding from the cell membranes into the extracellular space. In the case of GAD-BPI, it is a conjugate between P 208-217 peptide and LABL peptide (Table 1) (Tibbetts et al, 1999;Tibbetts et al, 2000). Using the distance estimate, a combination of glycine (G) and amino caproic acid (Acp) was used to connect LABL to GAD peptides.…”

Section: Design Of Novel Gad-bpi For Suppressing T1dmentioning

confidence: 99%

Peptides and Proteins for Treatment and Suppression of Type 1 Diabetes

Badawi¹,

Büyüktimkin²,

Kiptoo³

et al. 2011

Type 1 Diabetes - Pathogenesis, Genetics and Immunotherapy

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Peptides Derived From Icam-1 and Lfa-1 Modulate T Cell Adhesion and Immune Function in a Mixed Lymphocyte Culture1

Abstract: Our data suggest that these peptides or their derivatives may be useful as therapeutic modulators of LFA-1/ICAM-1 interaction during organ transplants.

Cited by 44 publications

References 35 publications

Stimulation Through Intercellular Adhesion Molecule-1 Provides a Second Signal for T Cell Activation

Stimulation Through Intercellular Adhesion Molecule-1 Provides a Second Signal for T Cell Activation

Intercellular adhesion molecule 1-dependent activation of interleukin 8 expression in Candida albicans-infected human gingival epithelial cells

Peptides and Proteins for Treatment and Suppression of Type 1 Diabetes

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