Intercellular Adhesion Molecule-1 (ICAM-1) and Lymphocyte Function-associated Antigen-1 (LFA-1) Contribute to the Elimination of Equine Herpesvirus Type 1 (EHV-1) from the Lungs of Intranasally Infected BALB/c Mice

Background: Equine herpesvirus type 1 (EHV-1) is the most important viral pathogen of equines, causing respiratory illness, abortion, neonatal foal mortality and neurologic disorders. Large numbers of commercial EHV-1 vaccines are available to protect equines from the disease, but they provide only partial protection. Despite immunization with inactivated and modified live virus vaccine, mares show abortions. Present study was aimed to investigate the immunogenicity and protective efficacy of EHV-1 recombinant glycoprotein B (rgB) and gB expressing plasmid DNA against EHV-1 infection in BALB/c mice model.Methods: About 3-4 weeks old 225 female BALB/c mice were selected for the comparative study of immunization followed by challenged with EHV-1/India/Tohana/96-2 strain virus in 5 different groups of 45 animals each.Result: Following immunization, rgB vaccinated mice showed optimal stimulation of EHV-1 gB specific cell mediated and humoral mediated immunity (HMI and CMI). The gB expressing plasmid DNA vaccinated mice developed only CMI while inactivated whole virus vaccinated mice had only HMI. Upon EHV-1 challenge, all infected mice displayed variable levels of clinical signs with changes in body weight, however, vaccinated mice showed very rapid recovery with optimal protection. Positive control group mice showed severe pulmonary lesions along with persistence virus infection till 5 days post challenge (dpc) whereas vaccinated mice had less pulmonary lesion only up to 3dpc. Minimal lung lesions and early virus clearance was observed in the rgB immunized mice in comparison to the gB plasmid DNA and inactivated EHV-1 vaccine immunized mice. It has been concluded that immunization with rgB elicits optimum protective immune response against EHV-1 infection in mice model. The rgB could be a potential vaccine candidate against EHV-1 infection in equine in the future.

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Adhesion of peripheral blood mononuclear cells and CD4+ T cells from patients with psoriasis to cultured endothelial cells via the interaction between lymphocyte function-associated antigen type 1 and intercellular adhesion molecule 1

British Journal of Dermatology ◽

10.1111/j.1365-2133.2007.08039.x ◽

2007 ◽

Vol 157 (2) ◽

pp. 259-265 ◽

Cited By ~ 14

Author(s):

D. Watabe ◽

H. Kanno ◽

A. Yoshida ◽

A. Kurose ◽

T. Akasaka ◽

...

Keyword(s):

T Cells ◽

Endothelial Cells ◽

Adhesion Molecule ◽

Mononuclear Cells ◽

Intercellular Adhesion Molecule ◽

Lymphocyte Function ◽

Intercellular Adhesion Molecule 1 ◽

Peripheral Blood Mononuclear ◽

Blood Mononuclear Cells

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Contribution of lymphocyte function-associated-1/intercellular adhesion molecule-1 binding to the adhesion/signaling cascade of cytotoxic T lymphocyte activation.

Journal of Experimental Medicine ◽

10.1084/jem.179.1.359 ◽

1994 ◽

Vol 179 (1) ◽

pp. 359-363 ◽

Cited By ~ 26

Author(s):

B Ybarrondo ◽

A M O'Rourke ◽

A A Brian ◽

M F Mescher

Keyword(s):

Adhesion Molecule ◽

Cytotoxic T Lymphocyte ◽

Lymphocyte Activation ◽

Cell Receptor ◽

Intercellular Adhesion ◽

Intercellular Adhesion Molecule ◽

Lymphocyte Function ◽

Intercellular Adhesion Molecule 1 ◽

Rapid Induction ◽

Blocking Effects

A rapid induction of adhesion to immobilized intercellular adhesion molecule (ICAM)-1 occurs when cytotoxic T lymphocytes (CTL) are stimulated with either soluble anti-T cell receptor (TCR) monoclonal antibodies (mAb) or with immobilized alloantigen, and this binding is blocked by the addition of anti-lymphocyte function-associated (LFA)-1 mAbs. Requirements for activating LFA-1 adhesion to ICAM-1 are similar to those found for induction of binding to immobilized fibronectin (FN), but distinct from those for activating CD8-mediated adhesion to class I major histocompatibility complex. A distinct role for LFA-1 in co-signaling for TCR-dependent degranulation could not be demonstrated. In contrast, both CD8 and the FN-binding integrin provide costimulatory signals for this response. Thus, if co-signaling via LFA-1 occurs, it clearly differs from that provided by CD8 or the FN-binding integrin. On the basis of antibody blocking effects, alloantigen-dependent activation of adhesion to ICAM-1 involves both the TCR and CD8. These results support a view of CTL activation as a cascade of adhesion and signaling events, with different coreceptors making distinct contributions.

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