PETER I. LOBO, M.D.
Osteopathic Medicine at Hospital Dr, Charlottesville, VA

6610834, Aug 26, 2003

Oct 10, 2000

09/684813

Peter I. Lobo - Charlottesville VA 22911

C07K 1600

5303896, 5303891, 4241361, 4241391, 4241301

Human sera from normal (i. e. , non-HIV infected) individuals contain certain IgM autoantibodies reactive to chemokine and other lymphocyte-surface receptors. A subset of these IgM autoantibodies that bind to such receptors, particularly CXCR4 and CCR5 receptors, can inhibit HIV-1 from infecting cells. Progression from an asymptomatic HIV-1 infected state to AIDS is determined in part by the level of IgM autoantibodies that inhibit HIV-1 from infecting cells. The claimed invention described herein is a method of using these isolated antibodies for the inhibition of the progression of virus-mediated diseases.

2008011, May 22, 2008

Jan 23, 2008

12/009912

Peter Lobo - Charlottesville VA, US

A61K 39/395, A61P 35/00, A61K 35/12, C12P 21/00, G01N 33/566, G01N 33/53, C07K 16/24, A61P 29/00

424172100, 424093700, 530389100, 435070300, 435007240, 436501000

Human and animal serum contains naturally occurring autoantibodies that develop at birth in absence of deliberate immunization. These antibodies are predominantly of IgM isotype but can include all immunoglobulin isotypes such as IgD, IgA and IgG. Here we describe IgM anti-lymphocyte autoantibodies (IgM-ALA) and show that these antibodies are heterogenous with some antibodies binding to chemokine receptors such as CCR5 and CXCR4 and others binding to other lymphocyte receptors including CD3, CD2, CD4 and CD81. These IgM-ALA, unlike IgG antibodies, are not cytolytic to cells at 37 C and hence function to alter lymphocyte function including cytokine production and act as “blocking antibodies to inhibit binding of chemokines and viruses including HIV-1 and Hepatitis C. IgM antibodies that bind to receptors on lymphocyte also bind to the same or similar class of receptors on other leucocytes and other cells such as cancer cells and endothelial cells. The inventor claims that naturally occurring anti-lymphocyte antibodies inhibit viral infections, cancer and several inflammatory states by binding to chemokine receptors and other cell membrane receptors that activate cells or promote viral entry and replication. Inventor also claims methods for quantitating levels of IgM-ALA with different receptor specificities to aid in preventing disease progression and also claims methods to enhance in-vivo or in-vitro production of IgM-ALA.

2008011, May 15, 2008

Jan 14, 2008

12/008778

Peter Lobo - Charlottesville VA, US

A61K 39/395

424131100, 424133100

Human and animal serum contains naturally occurring autoantibodies that develop at birth in absence of deliberate immunization. These antibodies are predominantly of IgM isotype but can include all immunoglobulin isotypes such as IgD, IgA and IgG. Here we describe IgM anti-lymphocyte autoantibodies (IgM-ALA) and show that these antibodies are heterogenous with some antibodies binding to chemokine receptors such as CCR5 and CXCR4 and others binding to other lymphocyte receptors including CD3, CD2, CD4 and CD81. These IgM-ALA, unlike IgG antibodies, are not cytolytic to cells at 37 C and hence function to alter lymphocyte function including cytokine production and act as “blocking antibodies to inhibit binding of chemokines and viruses including HIV-1 and Hepatitis C. IgM antibodies that bind to receptors on lymphocyte also bind to the same or similar class of receptors on other leucocytes and other cells such as cancer cells and endothelial cells. The inventor claims that naturally occurring anti-lymphocyte antibodies inhibit viral infections, cancer and several inflammatory states by binding to chemokine receptors and other cell membrane receptors that activate cells or promote viral entry and replication. Inventor also claims methods for quantitating levels of IgM-ALA with different receptor specificities to aid in preventing disease progression and also claims methods to enhance in-vivo or in-vitro production of IgM-ALA.

2005022, Oct 6, 2005

May 31, 2005

11/139566

Peter Lobo - Charlottesville VA, US

A61K039/395

424143100

In this invention, the inventor discloses that naturally occurring IgM anti-lymphocyte antibodies bind to chemokine and non-chemokine receptors on lymphocytes and other cells, and downmodulate certain receptors including CD4 and CD2 on T cells and CD80 and CD86 on macrophages. The inventor also discloses that such antibodies (i) inhibit HIV-1 and other viruses from infecting cells (ii) inhibits activation and proliferation of T lymphocytes (iii) inhibits cytokine and chemokine production (iv) inhibits inflammatory processes, and (v) enhances death of malignant cells. This art or invention is novel in that the antibodies described herein are “naturally occurring” i.e. develop in absence of deliberate immunization and secondly these antibodies are distinct from disease causing autoantibodies in that these naturally occurring antibodies are polyreactive with low binding affinity.

2003009, May 29, 2003

Nov 7, 2002

10/292002

Peter Lobo - Charlottesville VA, US

A61K039/395

424/144100

Human and animal serum contains naturally occurring autoantibodies that develop at birth in absence of deliberate immunization. These antibodies are predominantly of IgM isotype but can include all immunoglobulin isotypes such as IgD, IgA and IgG. Here we describe IgM anti-lymphocyte autoantibodies and show that these antibodies are heterogenous with some antibodies binding to chemokine receptors such as CCR5 and CXCR4 and others binding to other T cell receptors including CD3. IgM antibodies inhibit HIV-1 from infecting cells, inhibit chemokine from binding to receptors and inhibit activation and proliferation of T lymphocytes. IgM antibodies that bind to lymphocyte also bind to other leucocytes and other cells such as cancer cells and endothelial cells. The inventor claims that naturally occurring anti-lymphocyte antibodies of all immunoglobulin isotypes inhibit viral infections, cancer and several inflammatory states by binding to chemokine receptors and other cellular receptors that activate cells or promote viral entry.

5962239, Oct 5, 1999

May 6, 1997

8/852095

Peter I. Lobo - Charlottesville VA

The University of Virginia Patent Foundation - Charlottesville VA

G01N 33533

435 724

An improved method for detecting even low titer HLA antibodies in proposed organ transplant recipients employs flow cytometry crossmatching (FCXM) on pronase-treated B-cells and T-cells of the donor. Two-color FCXM is preferably employed. The peripheral blood lymphocytes, after pronase digestion, are maintained under conditions to suppress Fcy R receptor regeneration, combined with sera of the proposed transplant recipient, and tested against control sera, using fluorescent reporting complexing agents. Use of pronase digested lymphocytes permits the assay to distinguish between normal or irrelevant IgG B cell binding and immunologically important HLA antibody binding.