Abstract: A previously unrecognized fundamental property of ?1PI is to regulate the phenotypic composition of circulating and tissue-associated cells derived from hematopoietic stem cells. The present invention comprises screening for various unmodified and modified ?1PI's which are useful in the treatment of abnormalities in the number of cells of myeloid or lymphoid lineage that are associated with HIV-1 infection, microbial infection, leukemia, solid tumor cancers, atherosclerosis, autoimmunity, stem cell transplantation, organ transplantation, and other diseases affected by cells of the immune system. The interaction of ?1PI with its receptors, HLECS and LRP, influences the level of cells of different lineages. Genetic and proteolytic modification of ?1PI is used to target these receptors to increase or decrease specific cell populations, as needed, in the various disease states.

Abstract: In order to accurately and reliably quantitate HLE on the plasma membranes of the lymphocytes and mononuclear phagocytes, a test sample containing the lymphocytes and mononuclear phagocytes is initially treated with a first antiserum specific for CD4 receptors on the plasma membrane or with a second antiserum specific for chemokine receptors on the plasma membrane. Once the CD4 or chemoline receptors have been rendered non-reactive (competitive) relative to the HLE receptors (also “binding sites”) on the plasma membrane, the test sample is contacted with an immunoreagent specific for interaction with one or more of the HLE receptors on the plasma membranes of the lymphocytes and mononuclear phagocytes. The immunoreagent forms a complex with the HLE binding sites and produces a characteristic physical change in the lymphocytes and mononuclear phagocytes that can be monitored by anyone of a number of standard techniques, (e.g., confocal laser scanning microscopy and flow cytometry).

Abstract: A method for modulation of plasma membrane associated Human Leukocyte Elastase (HLE) to inflammatory states by interaction of HLE with an antagonist to inhibit HLE and thereby interruption in plasma associated events (e.g. HIV disease progression, bacterial infections and autoimmune diseases), which are responsive/sensitive to such inflammation. The antagonist suitable for use in this invention is designed to interact with each of the catalytic triad of the HLE plasma membranes protein and the lipid interactive amino acids of the HLE plasma membrane protein.

Abstract: In order to accurately and reliably quantitate HLE on the plasma membranes of the lymphocytes and mononuclear phagocytes, a test sample containing the lymphocytes and mononuclear phagocytes is initially treated with a first antiserum specific for CD4 receptors on the plasma membrane or with a second antiserum specific for chemokine receptors on the plasma membrane. Once the CD4 or chemokine receptors have been rendered non-reactive (competitive) relative to the HLE receptors (also “binding sites”) on the plasma membrane, the test sample is contacted with an immunoreagent specific for interaction with one or more of the HLE receptors on the plasma membranes of the lymphocytes and mononuclear phagocytes. The immunoreagent forms a complex with the HLE binding sites and produces a characteristic physical change in the lymphocytes and mononuclear phagocytes that can be monitored by any one of a number of standard techniques, (e.g., confocal laser scanning microscopy and flow cytometry).