|Specificity:||The antibody MEM-25 reacts with CD11a (alpha subunit of human LFA-1), a 170-180 kDa type I transmembrane glycoprotein expressed on B and T lymphocytes, monocytes, macrophages, neutrophils, basophils and eosinophils.
HLDA IV; WS Code NL 209
|Immunogen:||Leukocytes from a pacient suffering from a LGL-type leukaemia.|
|Preparation:||The purified antibody is conjugated with Fluorescein isothiocyanate (FITC) under optimum conditions. The reagent is free of unconjugated FITC and adjusted for direct use. No reconstitution is necessary.|
|Storage Buffer:||The reagent is provided in stabilizing phosphate buffered saline (PBS) solution containing 15mM sodium azide.|
|Storage / Stability:||Store in the dark at 2-8°C. Do not freeze. Avoid prolonged exposure to light. Do not use after expiration date stamped on vial label.|
|Usage:||The reagent is designed for Flow Cytometry analysis of human blood cells using 20 μl reagent / 100 μl of whole blood or 106 cells in a suspension.
The content of a vial (0.5 ml) is sufficient for 25 tests.
|Expiration:||See vial label|
|Lot Number:||See vial label|
|Background:||CD11a (LFA-1 alpha) together with CD18 constitute leukocyte function-associated antigen 1 (LFA-1), the alphaLbeta2 integrin. CD11a is implicated in activation of LFA-1 complex. LFA-1 is expressed on the plasma membrane of leukocytes in a low-affinity conformation. Cell stimulation by chemokines or other signals leads to induction the high-affinity conformation, which supports tight binding of LFA-1 to its ligands, the intercellular adhesion molecules ICAM-1, -2, -3. LFA-1 is thus involved in interaction of various immune cells and in their tissue-specific settlement, but participates also in control of cell differentiation and proliferation and of T-cell effector functions. Blocking of LFA-1 function by specific antibodies or small molecules has become an important therapeutic approach in treatment of multiple inflammatory diseases. For example, humanized anti-LFA-1 antibody Efalizumab (Raptiva) is being used to interfere with T cell migration to sites of inflammation; binding of cholesterol-lowering drug simvastatin to CD11a allosteric site leads to immunomodulation and increase in lymphocytic cholinergic activity.|
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*And many other.
For laboratory research only, not for drug, diagnostic or other use.
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