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The good, the (not so) bad and the ugly of immune homeostasis in melanoma

journal contribution
posted on 20.09.2021, 07:27 by Jessica da Gama DuarteJessica da Gama Duarte, Katherine Woods, Miles AndrewsMiles Andrews, Andreas BehrenAndreas Behren
Within the immune system multiple mechanisms balance the need for efficient pathogen recognition and destruction with the prevention of tissue damage by excessive, inappropriate or even self-targeting (auto)immune reactions. This immune homeostasis is a tightly regulated system which fails during tumor development, often due to the hijacking of its essential self-regulatory mechanisms by cancer cells. It is facilitated not only by tumor intrinsic properties, but also by the microbiome, host genetics and other factors. In certain ways many cancers can therefore be considered a rare failure of immune control rather than an uncommon or rare disease of the tissue of origin, as the acquisition of potentially oncogenic traits through mutation occurs constantly in most tissues during proliferation. Normally, aberrant cells are well-controlled by cell intrinsic (repair or apoptosis) and extrinsic (immune) mechanisms. However, occasionally oncogenic cells survive and escape control. Melanoma is one of the first cancer types where treatments aimed at restoring and enhancing an immune response to regain control over the tumor have been used with various success rates. With the advent of “modern” immunotherapeutics such as anti-CTLA-4 or anti-PD-1 antibodies that both target negative immune-regulatory pathways on immune cells resulting in durable responses in a proportion of patients, the importance of the interplay between the immune system and cancer has been established beyond doubt.

Funding

JGD is supported by a Tour de Cure Scott Canner Young Research Grant. MCA is supported by a NHMRC CJ Martin Fellowship (#1148680). The Olivia Newton-John Cancer Research Institute acknowledges the support of the Victorian Government Operational Infrastructure Support Program.

History

Publication Date

01/05/2018

Journal

Immunology and Cell Biology

Volume

96

Issue

5

Pagination

10p. (p. 497-506)

Publisher

Wiley

ISSN

0818-9641

Rights Statement

The Author reserves all moral rights over the deposited text and must be credited if any re-use occurs. Documents deposited in OPAL are the Open Access versions of outputs published elsewhere. Changes resulting from the publishing process may therefore not be reflected in this document. The final published version may be obtained via the publisher’s DOI. Please note that additional copyright and access restrictions may apply to the published version.

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