Tumor Necrosis Factor-α

CPT: 83520
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Synonyms

  • Cachectin

Expected Turnaround Time

3 - 7 days


Related Documents


Specimen Requirements


Specimen

Serum, frozen


Volume

1 mL


Minimum Volume

0.4 mL (Note: This volume does not allow for repeat testing.)


Container

Red-top tube or gel-barrier tube


Collection

Allow blood sample collected in serum separator tube to clot at room temperature for 30 minutes prior to centrifugation. Allowing samples to sit on the clot for more than 30 minutes may result in higher TNF-alpha levels.

Transfer the serum into a Labcorp PP transpak frozen purple tube with screw cap (Labcorp No. 49482). Freeze immediately and maintain frozen until tested. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested


Storage Instructions

Freeze.


Stability Requirements

Temperature

Period

Frozen

9 days

Freeze/thaw cycles

Stable x2


Causes for Rejection

Nonfrozen specimen; nonserum specimen; gross lipemia; gross hemolysis


Test Details


Use

This test is used for measurement of Tumor Necrosis Factor-α levels in serum.


Limitations

This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.


Methodology

Enzyme-linked immunosorbent assay (ELISA)


Reference Interval

0.0−2.2 pg/mL


Additional Information

Cytokines are low-molecular-weight intercellular signaling molecules.1-4 Cytokines are produced de novo in response to an immune stimulus. They regulate immune cell homeostasis by mediating innate and acquired immunity, and inflammation in human health and disease. They generally (although not always) act over short distances and short time spans and at very low concentrations. They act by binding to specific membrane receptors, which then signal the cell via second messengers, often tyrosine kinases, to alter its behavior. Responses to cytokines include increasing or decreasing expression of membrane proteins (including cytokine receptors), proliferation and secretion of effector molecules. It is common for different cell types to secrete the same cytokine or for a single cytokine to act on several different cell types (pleiotropy). Cytokines are redundant in their activity, meaning similar functions can be stimulated by different cytokines. Cytokines are often produced in a cascade, as one cytokine stimulates its target cells to make additional cytokines. Cytokines can also act synergistically (two or more cytokines acting together) or antagonistically (cytokines causing opposing activities).

Tumor necrosis factor-alpha (TNF-α) is an important pleiotropic cytokine involved in host defense, inflammation, and apoptosis.3 Local increases in TNF-α concentrations cause the five cardinal signs of inflammation: heat, swelling, redness, pain and loss of function.3 TNF-α was initially identified as a serum factor that could induce the hemorrhagic necrosis of tumors in patients following acute bacterial infections.5 TNF-α is a central cytokine in inflammatory reactions, and biologics that neutralize TNF are among the most successful drugs for the treatment of chronic inflammatory and autoimmune pathologies.5 In recent years, it became clear that TNF-α drives inflammatory responses not only directly by inducing inflammatory gene expression but also indirectly by inducing cell death, instigating inflammatory immune reactions and disease development.5 It plays a double role in regulation of immune responses, acting both as a proinflammatory mediator, initiating a strong inflammatory response, and an immunosuppressive mediator, inhibiting the development of autoimmune diseases and tumorigenesis, and exhibiting a vital role in maintenance of immune homeostasis by limiting the extent and duration of inflammatory processes.3 TNF-α plays an important role in host defense against viral, bacterial, fungal, and parasitic pathogens, in particular against intracellular bacterial infections, such as Mycobacterium tuberculosis and Listeria monocytogenes.3

High systemic TNF-α levels can lead to septic shock.3 TNF-α has been implicated in the development of allergic diseases, particularly asthma,6 and atopic dermatitis.7 Serum TNF-α results can be significantly increased in patients with systemic mastocytosis.8 The correlation coefficients between highly elevated histamine and cytokine concentrations during the acute phase were >95%, indicating the same cellular origin, possibly activated mast cells.8 Elevated TNF-α levels have been associated with worse survival in patients with severe COVID-19 infection.9-11 Elevated TNF-α levels have been observed in hospitalized patients with acute lung injury.12


Footnotes

1. Liu C, Chu D, Kalantar-Zadeh K, George J, Young HA, Liu G. Cytokines: From Clinical Significance to Quantification. Adv Sci (Weinh). 2021 Aug;8(15):e200443334114369
2. Chopp L, Redmond C, O'Shea JJ, Schwartz DM. From thymus to tissues and tumors: A review of T-cell biology. J Allergy Clin Immunol. 2023 Jan;151(1):81-97. Epub 2022 Oct 19.36272581
3. Akdis M, Aab A, Altunbulakli C, et al. Interleukins (from IL-1 to IL-38), interferons,transforming growth factor β, and TNF-α: Receptors, functions, and roles in diseases. J Allergy Clin Immunol. 2016 Oct;138(4):984-1010.27577879
4. Justiz Vaillant AA, Qurie A. Interleukin. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan.2022 Aug 22.29763015
5. van Loo G, Bertrand MJM. Death by TNF: a road to inflammation. Nat Rev Immuonl. 2023 May;23(5):289-303. Epub 2022 Nov 15.36380021
6. Brown SD, Brown LA, Stephenson S, et al. Characterization of a high TNF-α phenotypein children with moderate-to-severe asthma. J Allergy Clin Immunol. 2015 Jun;135(6):1651-1654.25725987
7. Zimmermann M, Koreck A, Meyer N, et al. TNF-like weak inducer of apoptosis (TWEAK) and TNF-α cooperate in the induction of keratinocyte apoptosis. J Allergy Clin Immunol. 2011 Jan;127(1):200-7, 207.e1-10.21211655
8. Boehm T, Ristl R, Mühlbacher J, Valent P, Wahrmann M, Jilma B. Massive release of TH2 cytokines induced acytokine storm during a severe mast cell activation event in a patient with indolent systemic mastocytosis. J Allergy Clin Immunol. 2022 Aug;150(2):406-414.35504498
9. Del Valle DM, Kim-Schulze S, Huang HH, et al. An inflammatory cytokine signature predicts COVID-19 severity and survival. Nat Med. 2020 Oct;26(10):1636-1643.32839624
10. Karki R, Sharma BR, Tuladhar S, et al. Synergism of TNF-alpha and IFN-gamma triggers inflammatory cell death, tissue damage, and mortality in SARS-CoV-2 infection andcytokine shock syndromes. Cell. 2021 Jan 7;184:149-168.e17.33278357
11. Chen G, Wu D, Guo W, et al. Clinical and immunological features of severe and moderate coronavirus disease 2019. J Clin Invest. 2020 May 1;130(5):2620-2629.32217835
12. Fremont RD, Koyama T, Calfee CS, et al. Acute lung injury in patients with traumatic injuries: utility of a panel of biomarkers for diagnosis and pathogenesis. J Trauma. 2010 May;68(5):1121-1127.20038857

LOINC® Map

Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
140673 Tumor Necrosis Factor-Alpha 3074-2 140682 Tumor Necrosis Factor-Alpha pg/mL 3074-2

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