As a famous expert with a high reputation in the complement field, Creative Biolabs is committed to the study of various molecular mechanisms and developing a variety of research platforms and protocols. Complement component C2 plays important roles in the complement system. Studies have shown that C2 deficiency is largely associated with a series of risks. Here, we describe the recombinant human C2 activity analysis protocol to promote your research. Please note that our protocols are only for your reference.
Recombinant Human C2 Activity Analysis
Fig.1 Flow chart of recombinant human C2 activity analysis. (Creative Biolabs)
Published Data
Fig.2 Recombinant human C2 (rhC2) reconstitutes classical pathway complement function in serum from patients lacking C2.1
To explore rhC2 as a treatment for diseases linked to C2 deficiency, its efficacy was tested in serum from individuals homozygous for C2 deficiency. The investigation employed a 3-pathway ELISA, assessing complement cascade activation, and a hemolytic assay, evaluating classical pathway activity by the serum's capacity to lyse antibody-coated sheep red blood cells. Effective activation of the classical pathway triggers membrane attack complex (MAC) assembly and consequent cell lysis. Serum from six C2-deficient patients supplemented with rhC2 underwent 3-pathway ELISA testing, with three samples also analyzed via the hemolytic assay. Titration of rhC2 determined that concentrations between 3.0 and 6.0 μg/ml restored ≥70% classical pathway activity compared to normal serum.
The human complement system is composed of a variety of different soluble and membrane proteins and plays an important role in both innate and adaptive immunity. In order to accelerate the project progress and research of our customers, Creative Biolabs has developed a series of products and services.
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Reference
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Martini, Paolo GV, et al. "Recombinant human complement component C2 produced in a human cell line restores the classical complement pathway activity in-vitro: an alternative treatment for C2 deficiency diseases." BMC Immunology 11 (2010): 1-10. Distributed under Open Access license CC BY 2.0, without modification.
For Research Use Only.
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