Efficacy of vaccination against influenza in patients with multiple sclerosis: The role of concomitant therapies

Pellegrino, Paolo; Carnovale, Carla; Perrone, Valentina; Pozzi, Marco; Antoniazzi, Stefania; Radice, Sonia; Clementi, Emilio

doi:10.1016/j.vaccine.2014.06.068

Cited by 36 publications

(20 citation statements)

References 42 publications

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“…However, use of natalizumab is limited in patients who are infected with the JC Virus, as they are at risk for progressive multifocal leukoencephalopathy, a fatal complication (69,70). Natalizumab-treated patients can also experience increased susceptibility to urinary and respiratory tract infections, which can trigger relapses (71).…”

Section: Discussionmentioning

confidence: 99%

Ena/VASP proteins regulate activated T-cell trafficking by promoting diapedesis during transendothelial migration

Estin

Thompson

Traxinger

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Vasodilator-stimulated phosphoprotein (VASP) and Ena-VASP-like (EVL) are cytoskeletal effector proteins implicated in regulating cell morphology, adhesion, and migration in various cell types. However, the role of these proteins in T-cell motility, adhesion, and in vivo trafficking remains poorly understood. This study identifies a specific role for EVL and VASP in T-cell diapedesis and trafficking. We demonstrate that EVL and VASP are selectively required for activated T-cell trafficking but are not required for normal T-cell development or for naïve T-cell trafficking to lymph nodes and spleen. Using a model of multiple sclerosis, we show an impairment in trafficking of EVL/VASP-deficient activated T cells to the inflamed central nervous system of mice with experimental autoimmune encephalomyelitis. Additionally, we found a defect in trafficking of EVL/VASP double-knockout (dKO) T cells to the inflamed skin and secondary lymphoid organs. Deletion of EVL and VASP resulted in the impairment in α4 integrin (CD49d) expression and function. Unexpectedly, EVL/VASP dKO T cells did not exhibit alterations in shear-resistant adhesion to, or in crawling on, primary endothelial cells under physiologic shear forces. Instead, deletion of EVL and VASP impaired T-cell diapedesis. Furthermore, T-cell diapedesis became equivalent between control and EVL/VASP dKO T cells upon α4 integrin blockade. Overall, EVL and VASP selectively mediate activated T-cell trafficking by promoting the diapedesis step of transendothelial migration in a α4 integrin-dependent manner.A ctivated T-cell trafficking across the vascular endothelium is essential for ongoing immune surveillance of tissues and for effective immune responses to conditions such as infection and cancer. Conversely, in situations of immune dysregulation, inhibition of self-reactive T-cell trafficking represents a promising target for therapeutic immunomodulation. Disruption of these pathways, such as by antibody blockade of α4 integrins, is a highly effective approach to immunomodulation (1, 2). However, the molecular mechanisms by which chemokine receptor and adhesion molecule signaling induce the T-cell cytoskeletal machinery to promote extravasation are not yet fully elucidated.Transendothelial migration (TEM), the process by which T cells extravasate from the blood into tissues, is characterized by four distinct steps: rolling along the vascular wall, arrest or adhesion, intravascular crawling, and diapedesis across the endothelial barrier (3). Surface adhesion molecules play well-characterized roles in each step of the process. For example, the initial rolling step of TEM is facilitated by interactions between T-cell and endothelial selectins, whereas the adhesion, intravascular crawling, and diapedesis steps of TEM are mainly regulated by chemokineand shear force-stimulated modulation of lymphocyte functionassociated antigen 1 (LFA-1, αLβ2 integrin, CD11a/CD18) and very late antigen 4 (VLA-4, α4β1 integrin, CD49d/CD29) interactions with intracellular adhesion molecule 1 ...

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Section: Discussionmentioning

confidence: 99%

Ena/VASP proteins regulate activated T-cell trafficking by promoting diapedesis during transendothelial migration

Estin

Thompson

Traxinger

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…Serum samples were obtained before vaccination with the trivalent seasonal influenza vaccine (≤21 days previously) been hypothesized to be the key mediators of the beneficial effects of daclizumab beta in MS. 4 As part of routine preventive care, patients with RRMS may require common inactivated vaccines, including seasonal influenza, 5 yet somewhat reduced response rates to the influenza vaccine have been observed in patients with RRMS treated with some immunomodulatory treatments. [6][7][8] Influenza in patients with MS can lead to hospitalizations and mortality. 9,10 Thus, it is important for physicians to have information about whether vaccinations can be performed safely and effectively during immunomodulatory treatment for MS.…”

Section: Vaccine Response Assessment and Endpointmentioning

confidence: 99%

Immune Response to Seasonal Influenza Vaccine in Patients with Relapsing-Remitting Multiple Sclerosis Receiving Long-term Daclizumab Beta

Mehta¹,

Umans²,

Ozen³

et al. 2017

International Journal of MS Care

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“…Unter Mitoxantron und Glatiramer-Aze-tat scheint zumindest auf die Influenza-Impfung ein vermindertes Ansprechen vorzuliegen [146].…”

Section: Neurologieunclassified

Impfungen bei Immundefekten/Immunsuppression – Expertenstatement und Empfehlungen

Wiedermann

Sitte

Burgmann

et al. 2016

Wien Klin Wochenschr

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Efficacy of vaccination against influenza in patients with multiple sclerosis: The role of concomitant therapies

Cited by 36 publications

References 42 publications

Ena/VASP proteins regulate activated T-cell trafficking by promoting diapedesis during transendothelial migration

Ena/VASP proteins regulate activated T-cell trafficking by promoting diapedesis during transendothelial migration

Immune Response to Seasonal Influenza Vaccine in Patients with Relapsing-Remitting Multiple Sclerosis Receiving Long-term Daclizumab Beta

Impfungen bei Immundefekten/Immunsuppression – Expertenstatement und Empfehlungen

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