• University of Mississippi 1955
• M.D., Tulane University Medical School, 1957

About Dr. Cooper:

Max Cooper received his medical degree and training in Pediatrics at Tulane University. While at the University of Minnesota, he worked with Robert Good to establish the dual nature of the adaptive immune system. With University of Alabama at Birmingham graduate student Paul Kincade, he discovered isotype switching by IgM-producing B cells. While on sabbatical at University College London, he worked with Martin Raff and John Owen to identify the precursors of B cells in mammalian bone marrow and fetal liver. His laboratory at Emory University investigates lymphocyte differentiation defects in immunodeficiency diseases and lymphoid malignancies, the role of Fc receptor-like molecules on human B cells, and the evolution of adaptive immunity.

Research Interests:

Fc Receptor-like Molecules on B cells. This immunology research laboratory has a long standing interest in normal B lymphocyte differentiation and defects thereof that result in immunodeficiencies, autoimmunity, or lymphoid malignancies. We and other investigators have identified a family of six genes, located near the classical FcR genes on human chromosome 1q21, that encode Fc receptor-like molecules (FcRL). They encode cell surface molecules with Ig-like extracellular domains, a transmembrane region, and cytoplasmic domains containing consensus immunoreceptor tyrosine-based activating and/or inhibitory motifs. The FcRL1-5 proteins are expressed at different stages in B cell differentiation. FcRL4, which has potent inhibitory potential, is expressed on a tissue-based subpopulation of memory B cells, where it may inhibit BCR-triggered proliferation to favor plasma cell differentiation and antibody production. Ongoing studies seek to define FcRL ligands, elaborate their function in antibody responses, and search for potential FcRL dysfunction in B cell malignancies, chronic infections and autoimmune diseases.

Phylogenetic Origin of Specific Adaptive Immunity. Since our initial delineation of the separate T and B cell lineages in birds, a long-standing question has been which cell type came first during evolution. Although all multicellular organisms possess innate immune defense mechanisms, only the jawed vertebrates have been found to have T, B, and antigen-presenting cells. In a search for insight into the origin of adaptive immunity, we have learned that two very different types of adaptive immune systems have evolved in vertebrates. The extant jawless vertebrates, lamprey and hagfish, have a lymphocyte antigen receptor repertoire that is potentially as large as our own antibody repertoire (>1014). However, unlike our Ig-based T cell receptors and B cell receptors for antigens, the variable lymphocyte receptors (VLR) of jawless vertebrates have an antigen-binding region formed by multiple leucine-rich-repeats (LRR) and are tethered to the lymphocyte surface by an invariant stalk region. The VLR genes are generated by a gene conversion mechanism involving a multistep, piece-wise assembly process through which flanking LRR sequences are stitched into an incomplete germline VLR gene. The VLR diversity is based on sequence differences and numbers of the constituent LRR modules. Monoallelic assembly and expression of unique VLR genes by individual lymphocytes results in the generation of clonally diverse lymphocyte populations, members of which can be selectively stimulated by bacteria, viruses, and mammalian cells to undergo activation, proliferation and differentiation into mature plasmacytes that produce multivalent VLR antibodies with precise specificity for protein and carbohydrate antigenic determinants. The remarkable antigen specificity, avidity, stability and ease of molecular engineering of the monoclonal VLR antibodies suggest they may have many biomedical uses, some of which we are currently exploring.