Lawrence Transfer Factor: Transference of Specific Immune Memory by Dialyzable Leukocyte Extract from a CD8+ T Cell Line.

Lawrence transfer factor (TF) is defined as dialyzable leukocyte extract (DLE) that can transfer antigen-specific cell-mediated immunity from a person testing positive for the antigen in a delayed type hypersensitivity skin test manner to a person negative for the same antigen. A recent article by Myles et al1 has identified a DLE isolated from an established CD8+ T cell line capable of transferring antigen-specific immunity. The DLE contains a portion of the beta chain of the T cell receptor and additional nucleotide and protein factors that are being subjected to further modern biochemical analysis. After months of study that included interviews of TF physician-scientists, we conclude that an antigen-specific TF exists for most, if not all, antigens. By working from a CD8+ T cell line with modern biochemical technology, it should be possible to identify and patent products capable of treating infectious diseases, antigen-responsive cancers, and autoimmune disorders.

Autochthonous Leprosy without Armadillo Exposure, Eastern United States.

Autochthonous leprosy has been reported in New York City, where there are no wild armadillos. Recent autochthonous cases also have been reported in Georgia and Florida and blamed on armadillos, including cases with no known armadillo exposure. International migration needs to be considered as a cause of autochthonous leprosy.

Leprosy as a model to understand cancer immunosurveillance and T cell anergy.

Leprosy is a disease caused by Mycobacterium leprae that presents on a spectrum of both clinical manifestations and T cell response. On one end of this spectrum, tuberculoid leprosy is a well-controlled disease, characterized by a cell-mediated immunity and immunosurveillance. On the opposite end of the spectrum, lepromatous leprosy is characterized by M. leprae proliferation and T cell anergy. Similar to progressive tumor cells, M. leprae escapes immunosurveillance in more severe forms of leprosy. The mechanisms by which M. leprae is able to evade the host immune response involve many, including the alterations of lipid droplets, microRNA, and Schwann cells, and involve the regulation of immune regulators, such as the negative checkpoint regulators CTLA-4, programmed death 1, and V-domain Ig suppressor of T cell activation-important targets in today's cancer immunotherapies. The means by which tumor cells become able to escape immunosurveillance through negative checkpoint regulators are evidenced by the successes of treatments, such as nivolumab and ipilimumab. Many parallels can be drawn between the immune responses seen in leprosy and cancer. Therefore, the understanding of how M. leprae encourages immune escape during proliferative disease states has potential to add to our understanding of cancer immunotherapy.

Quantiferon-Gold Tuberculosis Test Cannot Detect Latent Tuberculosis in Patients With Leprosy.

Five of 10 paucibacillary leprosy patients were Quantiferon Gold (Q-G) positive with negative chest X-rays. Forty multibacillary leprosy patients were negative. Reports have shown 100% cross-reactivity of ESAT6 and CFP10 between Mycobacterium leprae and Mycobacterium tuberculosis. The Q-G test cannot detect latent tuberculosis in patients with leprosy.