The role of dopamine receptors in lymphocytes and their changes in schizophrenia

Abstract

Dopamine and its 5 receptors, which are grouped into two families (D1-like and D2-like), modulate functions at a systemic level in both the central nervous system and periphery. The central nervous system and the immune system are the main adaptive systems, which participate in a continuous and functional crosstalk to guarantee homeostasis. On binding to its 5 dopamine receptors, dopamine acts as a co-regulator of the immune system, contributing to the interaction of the central nervous system and inflammatory events and as a source of communication between the different immune cells. Dopaminergic perturbations in the central nervous system are observed in several neurological and psychiatric disorders. Schizophrenia is one of the most common mental disorders with a poorly understood pathoaetiology that includes genetic and environmental components that promote alterations in the dopaminergic system. Interestingly, abnormalities in dopamine receptors expression in lymphocytes of schizophrenia patients have been reported, often significantly correlating with the severity of the psychotic illness. Here, we review the current literature regarding the dopaminergic system in human lymphocytes and its alterations in schizophrenia.

MiRNA Differences Related to Treatment-Resistant Schizophrenia

“…Experimental evidence, such as the association between the level of activation of the inflammatory response and schizophrenia, seems to suggest a role for stress in this condition [71][72][73][74]. Moreover, differences in this inflammatory response have also been noticed between schizophrenia and treatment-resistant schizophrenia [73,[75][76][77][78].…”

Dopamine, Immunity, and Disease

“…However, as peripheral immune cells are easily accessible in blood samples, these cells could potentially be used to monitor the status of homologous brain dopamine receptors ( Buttarelli et al, 2011 ; Tomasik et al, 2016 ). They may also be useful tools with which to monitor changes in dopamine receptor expression with respect to the efficacy of therapeutic interventions ( Buttarelli et al, 2011 ; Penedo et al, 2021 ). Using these types of data could enable a more nuanced usage of novel and repurposed anti-inflammatory and/or dopaminergic drugs as adjuvant therapies for schizophrenia and could provide novel targets and substantial improvements in the treatment and symptomatology involved in this disorder.…”

Microglia: The Real Foe in HIV-1-Associated Neurocognitive Disorders?

“…In 2017, Mlcochova et al showed that the absence of restriction by sterile alpha motif and histidine/aspartic acid domain-containing protein 1 (SAMDH1) restriction factor (RF) sterile alpha motif (SAM) was because it was phosphorylated by cyclin kinase 1 (CDK1), and it itself was induced in microglial cells cycling between G 0 to G 1 states [ 61 ] ( Table 1 ). Taken together, these clues indicate that microglia are infected by HIV-1 both in vitro and in vivo [ 20 ].…”

“…Macrophages or microglia can provoke the release of pr-inflammatory cytokines, including tumor necrosis factor α (TNFα), interferon α (IFNα), interleukin-6 (IL6), interleukin-8 (IL8), and interleukin-1β (IL1β) [ 6 , 8 , 13 ] ( Figure 1 ), as well as chemokines (C-C motif chemokine ligand 2 (CCL2) and C-C motif chemokine ligand 5 (CCL5), macrophage inflammatory protein 1β (MIP)-1β) [ 17 ]. These clues indicate the existence of cellular reservoirs in the CNS established within 3 to 5 days of HIV-1 infection [ 8 ], comprising three different types of long-lived infected cells [ 18 ]: astrocytes, monocyte lineage cells [ 19 ], and microglial cells [ 20 ].…”