tetano
Editor, Senior Moderator
JCI Insight. 2017 Jun 15;2(12). pii: 93222. doi: 10.1172/jci.insight.93222. [Epub ahead of print]
[h=1]Robust memory responses against influenza vaccination in pemphigus patients previously treated with rituximab.[/h] Cho A[SUP]1,[/SUP][SUP]2[/SUP], Bradley B[SUP]3[/SUP], Kauffman R[SUP]1,[/SUP][SUP]2[/SUP], Priyamvada L[SUP]1,[/SUP][SUP]2[/SUP], Kovalenkov Y[SUP]1,[/SUP][SUP]2[/SUP], Feldman R[SUP]3[/SUP], Wrammert J[SUP]1,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Rituximab is a therapeutic anti-CD20 monoclonal antibody widely used to treat B cell lymphoma and autoimmune diseases, such as rheumatic arthritis, systemic lupus erythematosus, and autoimmune blistering skin diseases (AIBD). While rituximab fully depletes peripheral blood B cells, it remains unclear whether some preexisting B cell memory to pathogens or vaccines may survive depletion, especially in lymphoid tissues, and if these memory B cells can undergo homeostatic expansion during recovery from depletion. The limited data available on vaccine efficacy in this setting have been derived from rituximab-treated patients receiving concomitant chemotherapy or other potent immunosuppressants. Here, we present an in-depth analysis of seasonal influenza vaccine responses in AIBD patients previously treated with rituximab, who generally did not receive additional therapeutic interventions. We found that, despite a lack of influenza-specific memory B cells in the blood, patients mount robust recall responses to vaccination, comparable to healthy controls, both at a cellular and a serological level. Repertoire analyses of plasmablast responses suggest that they likely derive from a diverse pool of tissue-resident memory cells, refractory to depletion. Overall, these data have important implications for establishing an effective vaccine schedule for AIBD patients and the clinical care of rituximab-treated patients in general and contribute to our basic understanding of maintenance of normal and pathogenic human B cell memory.
PMID: 28614800 DOI: 10.1172/jci.insight.93222
[h=1]Robust memory responses against influenza vaccination in pemphigus patients previously treated with rituximab.[/h] Cho A[SUP]1,[/SUP][SUP]2[/SUP], Bradley B[SUP]3[/SUP], Kauffman R[SUP]1,[/SUP][SUP]2[/SUP], Priyamvada L[SUP]1,[/SUP][SUP]2[/SUP], Kovalenkov Y[SUP]1,[/SUP][SUP]2[/SUP], Feldman R[SUP]3[/SUP], Wrammert J[SUP]1,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Rituximab is a therapeutic anti-CD20 monoclonal antibody widely used to treat B cell lymphoma and autoimmune diseases, such as rheumatic arthritis, systemic lupus erythematosus, and autoimmune blistering skin diseases (AIBD). While rituximab fully depletes peripheral blood B cells, it remains unclear whether some preexisting B cell memory to pathogens or vaccines may survive depletion, especially in lymphoid tissues, and if these memory B cells can undergo homeostatic expansion during recovery from depletion. The limited data available on vaccine efficacy in this setting have been derived from rituximab-treated patients receiving concomitant chemotherapy or other potent immunosuppressants. Here, we present an in-depth analysis of seasonal influenza vaccine responses in AIBD patients previously treated with rituximab, who generally did not receive additional therapeutic interventions. We found that, despite a lack of influenza-specific memory B cells in the blood, patients mount robust recall responses to vaccination, comparable to healthy controls, both at a cellular and a serological level. Repertoire analyses of plasmablast responses suggest that they likely derive from a diverse pool of tissue-resident memory cells, refractory to depletion. Overall, these data have important implications for establishing an effective vaccine schedule for AIBD patients and the clinical care of rituximab-treated patients in general and contribute to our basic understanding of maintenance of normal and pathogenic human B cell memory.
PMID: 28614800 DOI: 10.1172/jci.insight.93222