Reduction of Chemokine Secretion in Response to Mycobacteria in Infliximab-Treated Patients

Newton, Sandra M.; McDermott, Michael; Martineau, Adrian R.; Wilkinson, Katalin A.; Kampmann, Beate; Fisher, Corinne; Dutta, Shouma; Levin, Michael; Wilkinson, Robert J.; Pasvol, Geoffrey

doi:10.1128/cvi.00401-07

Cited by 31 publications

(20 citation statements)

References 37 publications

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“…Chemokine inhibition may have relevance for safety of anti-TNF therapy: infliximab reduced the secretion of IL-8/CXCL8, MIP-1-alpha/CCL3 and MCP-1/CCL2 in response to Mycobacteria. These authors suggest that the increased incidence of tuberculosis in infliximab-treated RA patients may be related, in part, to the inhibition of TNF-dependent chemokine gradients and impaired leukocyte migration (140). …”

Section: Targeting Of Chemoktnes and Chemoktne Receptorsmentioning

confidence: 99%

Chemokines and chemokine receptors in arthritis

Szekanecz¹

2010

Front Biosci

119

102

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Chemokines are involved in leukocyte recruitment to inflammatory sites, such as the synovial tissue in rheumatoid arthritis (RA). There is a structural and a functional classification of chemokines. The former includes four groups: CXC, CC, C and CX 3 C chemokines. Chemokines may also be either inflammatory or homeostatic, however, these functions often overlap. Antichemokine and anti-chemokine receptor targeting may be therapeutically used in the future biological therapy of arthritis. Most data in this field have been obtained from animal models of arthritis as only very few human RA trials have been completed. However, it is very likely that various specific chemokine and chemokine receptor antagonists will be developed and administered to RA patients.

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Section: Targeting Of Chemoktnes and Chemoktne Receptorsmentioning

confidence: 99%

Chemokines and chemokine receptors in arthritis

Szekanecz¹

2010

Front Biosci

119

102

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“…Then, the granuloma is able to attract specific or innate lymphocytes that would activate the infected macrophages, thus being an important defensive structure against M. tuberculosis infection, but that requires a constant chemokine production to persist [41]. These particularities in the onset of the infection provide an important window for constant endogenous reinfection even in the presence of protective immunity [40].…”

Section: The Mouse Model and Its Focus On Necrosis Formationmentioning

confidence: 99%

A Spotlight on Liquefaction: Evidence from Clinical Settings and Experimental Models in Tuberculosis

Cardona

2011

Clinical and Developmental Immunology

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Liquefaction is one of the most intriguing aspects of human tuberculosis. It is a major cause of the transition from the infection to active disease (tuberculosis, TB) as well as the transmission of M. tuberculosis to other persons. This paper reviews the natural history of liquefaction in humans from a pathological and radiological point of view and discusses how the experimental models available can be used to address the topic of liquefaction and cavity formation. Different concepts that have been related to liquefaction, from the influence of immune response to mechanical factors, are reviewed. Synchronic necrosis or apoptosis of infected macrophages in a close area, together with an ineffective fibrosis, appears to be clue in this process, in which macrophages, the immune response, and bacillary load interact usually in a particular scenario: the upper lobes of the lung. The summary would be that even if being a stochastic effect, liquefaction would result if the organization of the intragranulomatous necrosis (by means of fibrosis) would be disturbed.

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“…However, TNFα is a key cytokine in protective host defence against Mycobacterium tuberculosis ( M. tuberculosis ) and, together with TNF-dependent chemokines [34] play an important role in the development and maintenance of the granuloma which compartmentalises tubercle bacilli during infection [35,36] (Fig. 1).…”

Section: The Risk Of Incident Tuberculosis During Anti-tnf Therapymentioning

confidence: 99%

Screening for tuberculosis infection prior to initiation of anti-TNF therapy

Lalvani

Millington

2008

Autoimmunity Reviews

130

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T-cell interferon-gamma release assays (IGRAs) are more specific and probably more sensitive than the tuberculin skin test (TST) for the diagnosis of latent tuberculosis infection (LTBI). Patients with immune-mediated inflammatory diseases (IMID) and suspected LTBI who are candidates for anti-TNF therapy are at a significant risk of TB reactivation yet are prone to false-negative TST results because they are already on immunosuppressive medications. The role of these new blood tests in this patient population is therefore of considerable interest but is currently unclear. The limited published evidence-base shows that agreement between IGRA and TST results is poor in patients with IMID compared to patients without IMID, due to lower proportions of TST-positive results in patients with IMID. Discordant TST-positive, IGRA-negative results are associated with prior BCG vaccination and discordant TST-negative, IGRA-positive results are associated with steroid therapy. Notably, positive IGRA results are more closely associated with the presence of risk factors for LTBI than TST. The percentage of indeterminate IGRAs can be up to 12%. IGRA results in patients already taking anti-TNF agents currently remain uninterpretable. Given the clinical imperative to prevent reactivation of TB in patients starting anti-TNF therapy, screening algorithms should maximise diagnostic sensitivity for detection of LTBI. Therefore, a positive result to either an IGRA or TST, in addition to currently recommended clinical screening for risk factors for LTBI, should prompt consideration of preventive treatment of LTBI in this population.

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Reduction of Chemokine Secretion in Response to Mycobacteria in Infliximab-Treated Patients

Cited by 31 publications

References 37 publications

Chemokines and chemokine receptors in arthritis

Chemokines and chemokine receptors in arthritis

A Spotlight on Liquefaction: Evidence from Clinical Settings and Experimental Models in Tuberculosis

Screening for tuberculosis infection prior to initiation of anti-TNF therapy

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