C5-C9 (C5, C6, C7, C8, C9), Membrane Attack Complex (MAC)

Immunology

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Description

C5 to C9 ( including C6, C7 and C8 ) are the terminal components of all the complement pathways and together they form the membrance attack complex ( MAC ). This complex causes cell lysis in Gram-negative bacteria, but has no bactericidal effect in Gram-positive bacteria [1]. Reduced, but measurable concentrations of individual components are seen in chronic activation of the complement cascade, often in line with C3 and C4 changes, and C5-C9 measurement provides little additional clinical benefit [1]. The main clinical interest lies in the rare occurrence of genetic deficiency of any of the terminal components, in the absence of CH50. Ineffective MAC activity results in a susceptiblilty to Neisserial infection, particularly N.meningititis and N.gonorrhoeae. CH50 analysis and subsequent C5-C9 investigation should therefore be carried out in patients with recurrent meningitis or gonococcal episodes or a family history of severe meningitis [2]. However C9 deficiency if often asymptomatic and patients may have some CH50 activity.

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Indications

Absent CH50 and AP50. Recurrent or family history of Neiserrial Infections.

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Sample Type

2mL Fresh Serum ( Gel 5mL Yellow tube ). Separate within 2 hours of venesection and store at -20C.
Requests from outside Sheffield: freeze sample prior to dispatch and transport frozen sample at ambient temperature via Royal Mail or Courier ( dry ice not required ).

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Reference Range

Component | Normal range
C5 | 80 - 150 mg/L.
C6 | 40 - 80 mg/L.
C7 | 50 - 80 mg/L.
C8 | 40 - 280 mg/L.
C9 | 50 - 250 mg/L.

Reference ranges established in house and PRU collaboration.

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Turnaround Time

Within 5 weeks

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Testing Frequency

1 - 4 weeks

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External Notes

If there is going to be a delay in transporting the sample then 2ml Serum must be separated from clotted blood within 1-2 hours of venesection and stored at -20C as soon as possible. EDTA plasma samples should not be used as the chelation of calcium ions render some of the Complement components to be inactive. For typing of specific terminal complement pathway defects following screening with CH50.

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References

PRU Handbook of Clinical Immunochemistry. 9th Edition. 2007. [Ref 1]
Wen L, et al. Clinical and Laboratory evaluation of complement deficiency. Curr Rev All Clin Imm. 2004. 585-593. [Ref 2]
Walport MJ. Advances in Immunology: Complement First of Two Parts. N Engl J Med. 2001. 344:1058-1066.
Walport MJ. Advances in Immunology: Complement Second of Two Parts. N Engl J Med. 2001.344:1140-1144.

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Please note: the above information is subject to change and we endeavour to keep this website up to date wherever necessary.