Expression of costimulatory molecules (CD80, CD86, CD28, CD152), accessory molecules (TCR αβ, TCR γδ) and T cell lineage molecules (CD4+, CD8+) in PBMC of leprosy patients using Mycobacterium leprae antigen (MLCWA) with murabutide and T cell peptide of Trat protein

Peripheral blood responses to specific antigens and CD28 in sarcoidosis

“…29 Stimulation with M. leprae total cell wall antigen has been shown to decrease PBMC expression of CD28 and CD80 in patients with leprosy compared with healthy controls. 30 In sarcoidosis, evidence also indicates impairment of signal transduction pathways via the TCR/CD3 complex. Mechanisms include reduced expression of nuclear transcription factor NF-kB/p65 and lymphocyte-specific protein tyrosine kinase (p56 LCK ) in sarcoid CD4þ T-lymphocytes, with reduced INF-g and IL-2 production following polyclonal activation.…”

CD80/CD28 co-stimulation in human brucellosis

“…In other studies concerning patients with intracellular bacteria infections, differences have been noticed in the ex vivo expression of the co‐stimulatory molecules. Significantly low constitutive expression of CD80 and CD28 has been demonstrated on PBMC from lepromatous leprosy patients in which defective cellular immunity is the hallmark [25,26]. Moreover, pulmonary tuberculosis patients showed a decrease in the percentage of CD86 + monocytes compared to negative tuberculin test healthy subjects [30].…”

“…This hypothesis remains to be proved, as in the case of lepromatous leprosy. In these patients, in whom a defective cellular response is remarkable, diminished CD80/CD28 and increased CD152 expression in PBMC have been demonstrated [26].…”

“…This in vitro system allows the physiological cross‐talk between co‐stimulatory molecules and is more close to ‘natural’ infection. Moreover, detection of the cross‐regulation of co‐stimulatory molecules with flow cytometric analysis is reliable [25,26].…”

“…Because B7/CD28 molecules are critical in the initiation and maintenance of an effective T cell response, possible modulation of their expression by Brucella may provide a means of subverting the host immune response and favouring its survival. This concept has already been studied in other intracellular bacterial infections such as leprosy and tuberculosis [8,24–30].…”