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The nature of the association between polysaccharide and protein antigens in an intact bacterium versus a related conjugate vaccine critically determines the ability to generate memory for the polysaccharide‐specific IgG response
Author(s) -
Colino Jesus,
Chattopadhyay Gouri,
Sen Goutam,
Chen Quanyi,
Lees Andrew,
Canaday David H.,
Rubtsov Anatoly,
Torres Raul,
Snapper Clifford M.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.861.12
Subject(s) - conjugate , memory b cell , immunogen , antigen , biology , b cell , immunology , microbiology and biotechnology , streptococcus pneumoniae , antibody , chemistry , monoclonal antibody , antibiotics , mathematical analysis , mathematics
The capsular polysaccharide type 14 (PPS14) covalently linked to pneumococcal surface protein A (PspA) [conjugate] induces a memory IgG anti‐PPS14 response, in contrast to intact Streptococcus pneumoniae type 14 (Pn14). Nevertheless, the IgG anti‐PPS14 response to both conjugate and Pn14 are CD4+ T cell dependent. Pn14, in contrast to conjugate, fails to induce substantial B or T cell memory for the IgG anti‐PPS14 response, although both induce similar levels of PspA‐specific memory. Using lsc−/− mice we demonstrate that the IgG anti‐PPS14 response to Pn14 is dependent on marginal zone B (MZB) cells whereas the same response to conjugate utilizes follicular B (FB) cells. Nevertheless, conjugate linked to the surface of a non‐encapsulated Pn, depleted of PspA, can induce IgG anti‐PPS14 memory, but is now dependent on MZB. These data suggest that (i) the particulate nature of the immunogen is not the critical determinant for PPS14‐specific memory generation, and (ii) IgG PPS14‐specific memory can be generated in MZB, as well as FB cells. These data suggest instead, that the critical factor in the failure of Pn14 to generate PPS14‐specific memory may be the non‐covalent association of the bacterial proteins with PPS‐14, and subsequent failure to generate sufficient CD4+ T cell help for PPS14‐specific B cells.