Table 1 Characterization of mouse anti-mouse mAb against GPIbα and GPIIIa.

From: Desialylation is a mechanism of Fc-independent platelet clearance and a therapeutic target in immune thrombocytopenia

Clone name

IgG subtype

Antigen

Species cross-reactivity (tested)

Inhibits murine platelet aggregation

Inhibits human platelet aggregation

NIT A

IgG 2a

GPIbα

h, m, p

Yes

Yes

NIT B

IgG 2a

GPIbα

h, m, p

Yes

Yes

NIT F

IgG 2a

GPIbα

h, m, p

Yes

Yes

NIT E

IgG 2b

GPIbα

m

Yes

NA

NIT G

IgG 1

GPIbα

m

Yes

NA

NIT H

IgG 1

GPIbα

m

Yes

NA

9D2

IgG 1

GPIIbIIIa

h, m, p, r

Yes

No

M1

IgG 1

GPIIbIIIa

h, m, p, r

Yes

Yes

PSI B1

IgG 1

GPIIIa (PSI domain)

h, m, p, rib

Yes

Yes

PSI C1

IgG 1

GPIIIa (PSI domain)

h, m, p, rib

Yes

Yes

PSI E1

IgG 2b

GPIIIa (PSI domain)

h, m, p, rib

Yes

Yes

HUTA A

IgG 2a

GPIIbIIIa

h

NA

Yes

HUTA B

IgG 1

GPIIbIIIa

h, m, p

No

Yes

  1. IgG, immunoglobulin G; mAb, monoclonal antibody; NA, not applicable.
  2. mAbs were generated in GPIbα−/− and GPIIIa−/− mice. In addition to mouse (m), antibodies were also cross-reactive to other species, including tested human (h), pig (p), rat (r) and rabbit (rib). Antibodies cross-reactive with human antigens are in bold. ADP (20 μM)- or thrombin (1 U)-induced human/mouse platelet aggregation was inhibited by most anti-GPIIbIIIa mAbs. Ristocetin (20 μg ml−1)-/botrocetin (1.5 mg ml−1)-induced human/mouse platelet aggregation was inhibited by anti-GPIbα mAbs.
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