ANC28.1 mAb used as a Control in a Modified Chandler-loop model developed to screen and assess drug toxicity

ANC28.1 mAb used as a Control in a Modified Chandler-loop model developed to screen and assess drug toxicity This system could potentially prevent disastrous clinical human trials like the TGN1412 (anti-CD28) one.   “Extracorporeal human whole blood in motion as a tool to predict first-infusion reactions and mechanism-of-action of immunotherapeutics”  E A K Fletcher, S

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An important anti Cancer mechanism of CD279(PD-1) blockade elucidated

“PD-1 Blockade Promotes Epitope Spreading in Anti-cnacer CD8+ T cell Reponses by Preventing Fratricidal Death of Subdominant Clones To Relieve Immunodomination”  Arash Memarnejadian, S M Mansour Haeryfar, et al. (Nov 2017) J Immunol 199(9): 3348-59.  https://doi.org/10.4049/jimmunol.1700643.  PMID: 28939757   Often over time, an anti-Cancer immune response narrows into a few dominant (high affinity) CD8+ T

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Recombinant TIGIT Now Available!

New Ancell TIGIT-muIg binds to CD155 on U-937 cells and to recombinant CD155-muIg in EIA!   The TIGIT – CD155 regulatory pathway is emerging as an important element of immune function.  Studies using knockout mice demonstrate that this pathway is important in optimal NK effector cell function (activation and/or tolerance) (1) There is significant potential

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CD268 in BCP-ALL

CD268 (BAFF-R, TNFRSF13C) is a significant marker for B Cell Precursor Acute Lymphoblastic Leukemia (BCP-ALL). Ancell clone ANC268.2 was used to phenotype patient samples.  Blocking the BAFF – BAFFR pathway may prove to be useful in treating BCP-ALL.  “TNFRSF13C (BAFFR) positive blasts persist after early treatment and at relapse in childhood B-cell precursor acute lymphoblastic

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TIGIT – CD155 pathway

The TIGIT – CD155 regulatory pathway is emerging as an important element of immune function.  Studies using knockout mice demonstrate that this pathway is important in optimal NK effector cell function (activation and/or tolerance) (1) There is significant potential for the development of immunological drugs that could blockade this pathway, restoring anti-cancer immune response (2).

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