One year follow-ups of Chilean patients with COVID-19

Nova‐Lamperti, Estefania; Labarca, Gonzalo; Lastra, Jaime; Enos, Daniel

doi:10.1186/isrctn16865246

Cited by 1 publication

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“…It has been demonstrated that the functions of these two ligands are distinct and opposing with regards to T cell activation. [38][39][40][41] Manzotti and colleagues found that ligation of CTLA-4 with CD86 was associated with T cell proliferation, whereas ligation of CTLA-4 with CD80 resulted primarily in inhibition of T cell activation. 38 Based on these data, a model was proposed in which CD80 preferentially interacts with CTLA-4 in the absence of inflammatory stimuli, restricting T cell activation.…”

Section: Discussionmentioning

confidence: 99%

Autoantigen Tetramer Silences Autoreactive B Cell Populations

et al. 2020

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Many autoimmune therapies focus on immune suppression to reduce symptom severity and halt disease progression; however, currently approved treatments lack specificity for the autoantigen and rely on more global immune suppression. Multivalent antigen arrays can disarm pathogenic autoimmune B cell populations that specifically recognize the antigen of interest via their B cell receptor (BCR). Disarmament may be achieved by BCR engagement, crosslinking, and sustained receptor occupancy as a result of multivalent, high avidity BCR binding. To engage and explore this mechanism, a tetramer display of the encephalogenic proteolipid peptide (PLP 139-151 ), referred to as 4-arm PLP 139-151 , was synthesized by copper-catalyzed azide-alkyne cycloaddition chemistry. Subcutaneous administration of 4-arm PLP 139-151 completely ameliorated symptoms of paralysis in a mouse model of multiple sclerosis known as experimental autoimmune encephalomyelitis. Competitive binding of 4-arm PLP 139-151 to PLP 139-151 -specific IgG in mouse serum demonstrated the enhanced avidity associated with the multivalent array compared to free peptide. Furthermore, key PLP 139-151 -reactive B cells were depleted following 4-arm PLP 139-151 treatment, resulting in significant reduction of pro-inflammatory cytokines. Together, these data demonstrate the potential of 4-arm PLP 139-151 to silence autoreactive B cell populations and limit downstream activation of effector cells.

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