Development of protective long-lived antibody titre to antigens is a hallmark of successful vaccination. It is widely accepted that long-living plasma cells (LLPCs) residing in bone marrow are responsible for maintaining serum antibody titre. However, almost nothing is known how LLPCs are generated.
New research published in journal Immunity made observation that human LLPC population were selectively enriched in CD19-CD138+CD38+ population in bone marrow.
Initially the authors have sorted bone marrow populations enriched in plasmablast/ plasma cell markers from healthy volunteers. All 4 populations were making antibodies.
However, when analyzed for specific antibody production, the authors found that CD19-CD138+CD38+ subset was selectively enriched in antibody specificity against antigens encountered several years ago (e.g. mumps, measles, tetanus vaccine). In contrast, Flu-specific antibodies were secreted by several subsets.
To confirm this observation, the authors purified antigen-specific IgG from older volunteers and tested their origin using complementary mRNA sequences in subsets. This confirmed that long-lived antibody memory resided in CD19-CD138+CD38+ subset.
In summary, these results indicates that LLPCs in humans are residing in specialized bone marrow subset.
This is a observation study. It does not explain what signals would enhance CD19-CD138+CD38+ subset generation. One weakness of this paper is the fact that the authors did not follow LLPCs generation against naive (novel) antigens. Such experiment would have provided separate validation to their hypothesis.
David Usharauli
Initially the authors have sorted bone marrow populations enriched in plasmablast/ plasma cell markers from healthy volunteers. All 4 populations were making antibodies.
However, when analyzed for specific antibody production, the authors found that CD19-CD138+CD38+ subset was selectively enriched in antibody specificity against antigens encountered several years ago (e.g. mumps, measles, tetanus vaccine). In contrast, Flu-specific antibodies were secreted by several subsets.
In summary, these results indicates that LLPCs in humans are residing in specialized bone marrow subset.
This is a observation study. It does not explain what signals would enhance CD19-CD138+CD38+ subset generation. One weakness of this paper is the fact that the authors did not follow LLPCs generation against naive (novel) antigens. Such experiment would have provided separate validation to their hypothesis.
David Usharauli
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