CD48 Monoclonal Antibody K31 for Bone Marrow Transplantation: Functional Characteristics

Dreger, Peter; Mueller, Barbara M.; Schmitz, Norbert; Löffler, Hans; Müller-Ruchholtz, W

doi:10.1007/978-3-642-77083-8_37

Cited by 1 publication

(2 citation statements)

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“…Consequently, we used specific neutralizing antibodies for CD48, CD2, and 2B4 to investigate their roles in this experimental regimen ( Figures 4A-4F) (20)(21)(22)(23). These antibodies were also analyzed by us to determine whether they deplete targeted cells in vivo.…”

Section: Neutralization Of Cd48 Attenuates Eosinophilic Inflammationmentioning

confidence: 99%

“…Interestingly, whereas CD2-deficient mice display normal T cell development and function, CD48-deficient mice exhibit significant defects in CD4 ϩ T cell activation (13,14), indicating a broad immunologic role for CD48. Indeed, CD48 has been described as facilitating cell adhesion (15,16), innate responses to bacterial infection (17)(18)(19), and graft rejection (20)(21)(22)(23).…”

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confidence: 99%

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CD48 Is Critically Involved in Allergic Eosinophilic Airway Inflammation

Munitz

Bachelet²,

Finkelman³

et al. 2007

Am J Respir Crit Care Med

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Rationale: Despite ongoing research, the molecular mechanisms controlling asthma are still elusive. CD48 is a glycosylphosphatidylinositolanchored protein involved in lymphocyte adhesion, activation, and costimulation. Although CD48 is widely expressed on hematopoietic cells and commonly studied in the context of natural killer and cytotoxic T cell functions, its role in helper T cell type 2 settings has not been examined. Objectives: To evaluate the expression and function of CD48, CD2, and 2B4 in a murine model of allergic eosinophilic airway inflammation. Methods: Allergic eosinophilic airway inflammation was induced by ovalbumin (OVA)-alum sensitization and intranasal inoculation of OVA or, alternatively, by repeated intranasal inoculation of Aspergillus fumigatus antigen in wild-type, STAT (signal transducer and activator of transcription)-6-deficient, and IL-4/IL-13-deficient BALB/c mice. Gene profiling of whole lungs was performed, followed by Northern blot and flow cytometric analysis. Anti-CD48, -CD2, and -2B4 antibodies were administered before OVA challenge and cytokine expression and histology were assessed. Measurements and Main Results:Microarray data analysis demonstrated upregulation of CD48 in the lungs of OVA-challenged mice. Allergen-induced CD48 expression was independent of STAT-6, IL-13, and IL-4. Neutralization of CD48 in allergen-challenged mice abrogated bronchoalveolar lavage fluid and lung inflammation. Neutralization of CD2 inhibited the inflammatory response to a lesser extent and neutralization of 2B4 had no effect. Conclusions: Our results suggest that CD48 is critically involved in allergic eosinophilic airway inflammation. As such, CD48 may provide a new potential target for the suppression of asthma.

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Section: Neutralization Of Cd48 Attenuates Eosinophilic Inflammationmentioning

confidence: 99%