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Method of reducing and treating uvb-induced immunosuppressionUSPTO Application #: 20060142235Title: Method of reducing and treating uvb-induced immunosuppression Abstract: Methods of preventing and/or treating UV-induced immunosuppression by administration of immune response modifier compounds are disclosed herein. Suitable immune response modifier compounds include agonists of one or more TLRs. (end of abstract) Agent: 3m Innovative Properties Company - St. Paul, MN, US Inventors: Richard L. Miller, Anthony A. Gaspari, Joseph A. Gillis USPTO Applicaton #: 20060142235 - Class: 514044000 (USPTO) Related Patent Categories: Drug, Bio-affecting And Body Treating Compositions, Designated Organic Active Ingredient Containing (doai), O-glycoside, , Nitrogen Containing Hetero Ring, Polynucleotide (e.g., Rna, Dna, Etc.) The Patent Description & Claims data below is from USPTO Patent Application 20060142235. Brief Patent Description - Full Patent Description - Patent Application Claims RELATED APPLICATION DATA [0001] This application is a continuation of U.S. patent application Ser. No. 10/371,146, filed Feb. 20, 2003, which claims priority to U.S. Provisional Patent Application Ser. No. 60/358,982, filed Feb. 22, 2002. BACKGROUND OF THE INVENTION [0002] Human skin is an organ that protects the body from the influences of the external environment. A portion of that protective function is provided by an immune system specific to the skin--the so-called skin immune system--that protects the body from potentially harmful environmental influences including pathogens and transformed skin cells. The skin immune system may provide a localized response known as contact hypersensitivity (CHS), a systemic response known as delayed type hypersensitivity (DTH), or both. [0003] Exposing skin to ultraviolet radiation of the sun, particularly UV-B radiation, may damage certain types of cells involved in the skin immune system. Such damage may at least partially suppress function of the skin immune system and, therefore, may result in UV-induced immunosuppression. [0004] Langerhans cells are dendritic-like elements of the skin immune system that may function to present antigens to Th1-lymphocytes. Langerhans cells may be particularly affected by exposure to UV radiation. Exposure to UV radiation can cause changes in Langerhans cells that may contribute to UV-induced immunosuppression. For example, exposure to UV radiation may impair the ability of Langerhans cells to present antigens. [0005] Cytokines are known to be involved in the development of contact hypersensitivity (CHS) and the suppression of contact hypersensitivity by UV radiation. For example, interleukin (IL)-10 is a cytokine produced by keratinocytes after the keratinocytes are exposed to UV radiation. IL-10 impairs Langerhans cell function and suppresses CHS. Also, IL-12 promotes a Th1-lymphocyte immune response and is involved in the induction of CHS. IL-12 can reduce the immunosuppressive effects of UV radiation. Furthermore, administration of IL-12 prior to UV treatment may counteract UV-induced systemic suppression of delayed type hypersensitivity (DTH). [0006] Ectoin and ectoin derivatives may be used for the prophylaxis or treatment of UV-induced immunosuppression. Such compounds may be incorporated into compositions for topical administration. SUMMARY OF THE INVENTION [0007] In one aspect, the present invention provides a method of reducing UV-induced immunosuppression that includes administering to a treatment area an immune response modifier compound in an amount effective to inhibit UV-induced immunosuppression. [0008] In certain embodiments, the immune response modifier compound can be an agonist of at least one Toll-like receptor (TLR). For example, in some embodiments, the immune response modifier compound can include an imidazoquinoline amine, an imidazopyridine amine, a 6,7-fused cycloalkylimidazopyridine amine, a 1,2-bridged imidazoquinoline amine, an imidazonaphthyridine amine, an oxazoloquinoline amine, an imidazotetrahydronaphthyridine amine, a thiazoloquinoline amine, an oxazolopyridine amine, a thiazolopyridine amine, an oxazolonaphthyridine amine, or a thiazolonaphthyridine amine. In certain embodiments, the immune response modifier compound is administered via a topical application vehicle such as a cream, a gel, a spray, an ointment, a lotion, a solution, a suspension, an emulsion, a paste, a powder, or an oil. [0009] In another aspect, the present invention provides a method of treating UV-induced immunosuppression that includes administering to a treatment area an immune response modifier compound in an amount effective to inhibit UV-induced immunosuppression. In certain embodiments, the immune response modifier compound can be an agonist of at least one Toll-like receptor (TLR). For example, in some embodiments, the immune response modifier compound can include an imidazoquinoline amine, an imidazopyridine amine, a 6,7-fused cycloalkylimidazopyridine amine, a 1,2-bridged imidazoquinoline amine, an imidazonaphthyridine amine, an imidazotetrahydronaphthyridine amine, an oxazoloquinoline amine, a thiazoloquinoline amine, an oxazolopyridine amine, a thiazolopyridine amine, an oxazolonaphthyridine amine, or a thiazolonaphthyridine amine. [0010] In certain embodiments, the immune response modifier compound is administered via a topical application vehicle such as a cream, a gel, a spray, an ointment, a lotion, a solution, a suspension, an emulsion, a paste, a powder, or an oil. [0011] Various other features and advantages of the present invention should become readily apparent with reference to the following detailed description, examples, claims and appended drawings. In several places throughout the specification, guidance is provided through lists of examples. In each instance, the recited list serves only as a representative group and should not be interpreted as an exclusive list. BRIEF DESCRIPTION OF THE DRAWINGS [0012] FIG. 1 is a summary of the protocol for testing the contact hypersensitivity of mice treated with IRM before exposure to UV-B radiation; [0013] FIG. 2 is a bar graph summarizing the contact hypersensitivity of mice treated with IRM before exposure to UV-B radiation; [0014] FIG. 3 is a summary of the protocol for testing the contact hypersensitivity of mice treated with IRM after exposure to UV-B radiation; [0015] FIG. 4 is a bar graph summarizing the contact hypersensitivity of mice treated with IRM after exposure to UV-B radiation. DETAILED DESCRIPTION OF ILLUSTRATIVE EMBODIMENTS OF THE INVENTION [0016] Immune response modifiers ("IRMs") include compounds that possess potent immunostimulating activity including but not limited to antiviral and antitumor activity. Certain IRMs effect their immunostimulatory activity by inducing the production and secretion of cytokines such as, e.g., Type I interferons, TNF-.alpha., IL-1, IL-6, IL-8, IL-10, IL-12, MIP-1, and MCP-1. Certain IRMs are small organic molecules such as those disclosed in, for example, U.S. Pat. Nos. 4,689,338; 4,929,624; 5,266,575; 5,268,376; 5,352,784; 5,389,640; 5,482,936; 5,494,916; 6,110,929; 6,194,425; 4,988,815; 5,175,296; 5,367,076; 5,395,937; 5,693,811; 5,741,908; 5,238,944; 5,939,090; 6,039,969; 6,083,505; 6,245,776; 6,331,539; and 6,376,669; and PCT Publications WO 00/76505; WO 00/76518; WO 02/46188, WO 02/46189; WO 02/46190; WO 02/46191; WO 02/46192; WO 02/46193; and WO 02/46194. [0017] Additional small molecule IRMs include purine derivatives (such as those described in U.S. Pat. Nos. 6,376,501 and 6,028,076), small heterocyclic compounds (such as those described in U.S. Pat. No. 6,329,381), and amide derivatives (such as those described in U.S. Pat. No. 6,069,149). [0018] Other IRMs include large biological molecules such as oligonucleotide sequences. Some IRM oligonucleotide sequences contain cytosine-guanine dinucleotides (CpG) and are described, for example, in U.S. Pat. Nos. 6,1994,388; 6,207,646; 6,239,116; 6,339,068; and 6,406,705. Some CpG-containing oligonucleotides can include synthetic immunomodulatory structural motifs such as those described, for example, in U.S. Pat. Nos. 6,426,334 and 6,476,000. Other IRM nucleotide sequences lack CpG and are described, for example, in International Patent Publication No. WO 00/75304. [0019] Certain IRMs can function as Toll-like receptor (TLR) agonists, i.e., their immunomodulating influence is exerted through a TLR-mediated cellular pathway. For example, some small molecule IRMs have been identified as agonists of one or more of TLRs 2, 4, 6, 7, and 8; and CpG has been identified as an agonist of TLR9. In many cases, activating a TLR-mediated pathway results in gene transcription (e.g., cytokine or co-stimulatory marker expression) by activating NF-.kappa.B regardless of the particular TLR that is activated. Continue reading... Full patent description for Method of reducing and treating uvb-induced immunosuppression Brief Patent Description - Full Patent Description - Patent Application Claims Click on the above for other options relating to this Method of reducing and treating uvb-induced immunosuppression patent application. 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