DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Status of the Claims
Applicant’s submission filed on October 7, 2025 has been entered and considered. Rejections and/or objections not reiterated from the previous action mailed June 16, 2025 are hereby withdrawn. The following rejections and/or objections are either newly applied or are reiterated and are the only rejections and/or objections presently applied to the instant application. The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
The amended claims filed on October 7, 2025 are acknowledged. Claim 1 has been amended. Claims 4-13 have been canceled. Claim 14 has been newly added.
Claims 1-3 and 14 are pending and examined on the merits.
Priority
Acknowledgment is made of applicant’s claim for foreign priority based on application filed in the Republic of Korea on February 11, 2020. Receipt is acknowledged of certified copies of papers received in the original language as required by 37 CFR 1.55.
Information Disclosure Statement
The information disclosure statement (IDS) filed on August 11, 2022 is acknowledged and has been considered by the examiner.
Withdrawn Claim Rejections - 35 USC § 103
The prior rejection of claims 1-3 under 35 U.S.C. 103 as being unpatentable over Herz et al. (1998, A Human-SCID mouse model for allergic immune responses: bacterial superantigen enhances skin inflammation and suppresses IgE production, J. of Investigative Dermatology, 110(3), 224-231; found in IDS dated 08/11/2022) in view of Parker et al. (US 5,945,576) and Kobayashi et al. (US 2003/0185864 A1) is withdrawn in light of Applicant’s amendment to claim 1 to recite a method of generating an atopic dermatitis avatar mouse comprising the steps of (a) separating from peripheral blood mononuclear cells (PBMCs) isolated from a subject with atopic dermatitis CD3+ T cells and (1) CD3+ T cell-depleted peripheral blood mononuclear cells (CD3-depleted PBMCs), or (2) CD14+ monocyte cells and dendritic cells; and (b) injecting into an immunodeficient mouse (i) the CD3+ T cells; and (ii) (1) the CD3-depleted PBMCs, or (2) the CD14+ monocyte cells and the dendritic cells, wherein the CD3+ T cells are injected intravenously, and (1) the CD3-depleted PBMCs, or (2) the CD14+ monocyte cells and the dendritic cells are injected intradermally, Applicant’s cancellation of claims 4-13, and Applicant’s addition of claim 14.
Claim Rejections - 35 USC § 103
Claims 1-3 and 14 are rejected under 35 U.S.C. 103 as being unpatentable over Herz et al. (1998, A Human-SCID mouse model for allergic immune responses: bacterial superantigen enhances skin inflammation and suppresses IgE production, J. of Investigative Dermatology, 110(3), 224-231; found in IDS dated 08/11/2022, hereafter “Herz”) in view of Parker et al. (US 5,945,576, hereafter “Parker”).
This is a new rejection necessitated by applicant’s amendment. This rejection shares substantial similarity to the rejection as set forth in the previous office action dated June 16, 2025. Any aspect of Applicant’s traversal that pertains to the rejection as newly set forth will be provided following the new statement of rejection.
With regard to claims 1 and 14, Herz teaches a humanized mouse model for allergic immune responses wherein the model is generated by isolating PBMCs from atopic dermatitis patients sensitized to house dust mites and injecting the PBMCs into immunodeficient SCID mice (Abstract). Herz teaches wherein the injection of PBMCs were performed intraperitoneally and an additional injection of PBMCs from atopic dermatitis patients sensitized to house dust mites was given intradermally (Abstract, see also Pg. 225, Topical treatment of SCID mice). Herz teaches that the additional intradermal injection of PBMCs is required in order to produce epidermal and dermal skin inflammation in response to an allergen (Pg. 229, left col., 1st full para.). Herz further teaches wherein separation of CD14+ antigen presenting cells were isolated from PBMCs (Pg. 225, Isolation and removal of CD14+ cell subset) and CD14- PBMCs were administered to SCID mice, teaching that CD14+ antigen presenting cells are critical for the production of the allergenic IgE response (Pg 226, right col., last para.; Pg. 227, left col., 1st para.; see also Figure 4) which is indicative of atopic dermatitis (Pg. 224, left col. 2nd para.). Thus, Herz teaches intradermal injection of PBMCs in addition to intraperitoneal injection of PBMCs isolated from atopic dermatitis patients order to generate an atopic dermatitis response and teaches that CD14+ antigen presenting cells are important for generation of the allergen response in atopic dermatitis.
While Herz teaches systemic and intradermal injection of whole PBMCs, Herz does not teach separating CD3+ T cells and CD3-depleted PBMCs from the PBMCs isolated from a subject with atopic dermatitis, nor does Herz teach injection of CD3+ T cells and CD3-depleted PBMCs or CD14+ monocyte cells and dendritic cells wherein the CD3+ T cells are injected intravenously and the CD3-depleted PBMCS or CD14+ monocyte cells and dendritic cells are injected intradermally.
Parker teaches a method of generating a mouse model of an inflammatory skin condition via administration of isolated donor lymphocytes to an immune system deficient recipient animal (Col. 5, lines 1-5), wherein the inflammatory skin condition can be atopic dermatitis (Col. 5, line 17) and the immune system deficient recipient animal can be a SCID mouse (Col. 5, line 32). Parker teaches that the donor lymphocytes can be T-lymphocytes (Col. 6, line 10) which may either be “unfractionated or a subset” (Col. 6, line 12) and teaches a preferred embodiment wherein the donor T-lymphocytes are CD4+ or CD8+ (Col. 6, line 12), which is considered to reasonably read on CD3+ T cells. Parker teaches wherein the donor lymphocytes may be administered via “known methods”, including intravenous injection (Col. 10, lines 33-36). Thus, Parker teaches intravenous administration of CD3+ T-cells into an immunodeficient mouse. Additionally, Parker teaches that their method results in a mouse model exhibiting a phenotype of an inflammatory skin condition which is substantially the same as the phenotype in human disease (Col. 10, lines 45-49). Further, Parker teaches that their method, unlike existing animal models of inflammatory skin conditions, induces the inflammatory skin condition in “virtually all recipient animals” (Col. 5, lines 51-54 and lines 60-62; Col. 11, lines 26-30) and produces an animal model having an inflammatory skin condition that is “representative of the clinical and histopathological profile” of human disease (Col. 11, lines 50-51).
Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention, to apply Parker’s method of generating a mouse model of atopic dermatitis by intravenous injection of CD3+ T-lymphocytes to the “humanized” mouse model of atopic dermatitis generated by intraperitoneal and subcutaneous injections of PBMCs from subjects with atopic dermatitis taught by Herz. Parker teaches that their method results in a model more similar to human disease (Col. 10, lines 45-49 and Col. 11, lines 50-51) and wherein the inflammatory skin condition can be induced in nearly all recipient animals (Col. 5, lines 51-54 and lines 60-62 and Col. 11, lines 26-30). Thus, one having ordinary skill in the art would have been motivated to combine Parker’s method intravenous injection of CD3+ T-lymphocytes with Herz’s humanized atopic dermatitis mouse model generated by intraperitoneal and intradermal injections of PBMCs isolated from subjects having atopic dermatitis. A skilled artisan would have recognized that the combination would yield a “humanized” avatar-type mouse model exhibiting a similar phenotype to human disease via use of a method which is more reliable in inducing an inflammatory skin condition, leading to an improved animal model, increased efficiency, and reduced cost burden. One having ordinary skill in the art would have had a reasonable expectation of success as both Herz and Parker teach the generation of mouse models of atopic dermatitis.
Additionally, as Herz teaches that an intradermal injection of PBMCs is required to produce epidermal and dermal skin inflammation in response to an allergen and that CD14+ antigen presenting cells are important for generation of the allergen response in atopic dermatitis, it could be readily envisioned by a skilled artisan to substitute intradermal injection of CD14+ antigen presenting cells, which is considered to reasonably read on CD14+ monocyte cells and dendritic cells as per Claim 1, or CD3-depleted PBMCs which necessarily comprise CD14+ antigen presenting cells as per Claims 1 and 14, for the intradermal injection of PBMCs as taught by Herz with a reasonable expectation of success and with the predictable result of generating the allergen-induced epidermal and dermal skin inflammation which is a critical component of the claimed mouse model. A skilled artisan would have been motivated to make this substitution because Herz teaches CD14+ antigen presenting cells are important for generation of the allergen response in atopic dermatitis as per Claim 1, and in order to utilize the remainder of a blood sample procured from a patient after separating CD3+ cells thereby reducing the number of blood draws required from atopic dermatitis patients and providing increased experimental control via use of the same blood sample in order to generate the humanized mouse model as per Claims 1 and 14.
With regard to claim 2, Herz teaches that the atopic dermatitis is induced by house dust mites (Abstract).
With regard to claim 3, Herz teaches use of a SCID mouse (Abstract).
Response to Applicant’s Traversal
Applicant’s traversal filed on October 7, 2025 is acknowledged and has been fully considered but is not persuasive.
Applicant asserts on Pg. 5 of the traversal that the prior art combination of Herz and Parker does not teach or suggest intravenous injection of CD3+ T cells in combination of intradermal injection of antigen presenting cells (APCs). Applicant asserts that Herz does not teach injection of isolated CD14+ monocytes or dendritic cells to replicate disease pathology and instead teaches separation of CD 14+ APCs in order to assess their role in IgE production. Applicant asserts that the intradermal injection as taught in Herz is whole PBMCs and not isolated APCs as instantly claimed and thus would not teach or motivate a skilled artisan to reach the instantly claimed invention. Additionally, Applicant asserts that Parker does not cure the deficiencies of Herz as Parker does not teach the isolation of cellular subsets of PBMCs to be injected intravenously or intradermally. Applicant asserts that Parker teaches a method of inducing inflammatory skin conditions by injecting purified CD4+/CD45RB high T-lymphocytes into immunodeficient mice. Applicant asserts that Parker teaches removal of APCs from T-cells in their method of inducing inflammatory skin conditions which Applicant asserts teaches away from the method of the claimed invention. Applicant asserts that Herz and Parker disclose either the removal or use of unfractionated APCs and that since neither Herz nor Parker disclose the claimed method of generating a mouse model using isolated CD3+ T cells injected intravenously and isolated APCs injected intradermally, a skilled artisan would not be able to combine the prior art of Herz and Parker to arrive at the claimed invention.
Applicant’s arguments have been considered but are not found persuasive.
In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case, Herz teaches that intradermal injection is required in order to generate epidermal and dermal inflammatory response indicative of disease pathology (Pg. 229, left col., 2nd para.) and that CD14+ are required in order to produce an IgE response (Pg. 227, left col. 1st para.), which a skilled artisan would recognize is a critical part of replicating disease pathology. Therefore, it would be easily envisioned by a skilled artisan to use CD14+ APCs which Herz teaches are required for allergenic responses in an intradermal injection which Herz teaches is required for epidermal and dermal inflammatory response in a model replicating disease pathology. Further, Parker teaches isolation of a subset of T-lymphocytes to be injected intravenously in order to generate the mouse model of an inflammatory skin condition and provides CD4+ and CD8+ subsets as exemplary embodiments and teaches that “preparations of donor lymphocytes…can be provided in isolated form (i.e., removed from their naturally-occurring environment within an animal)” (Col. 8, lines 50-53). Thus, a skilled artisan would have recognized that CD3+ T-cells, which could be isolated from PBMCs, injected intravenously would be effective in generate the mouse model of an inflammatory skin condition. Further, although the method of Parker would involve removal of APCs in order to isolate CD3+ T-cells, Parker’s teachings are limited to intravenous injection of isolated CD3+ T-cells in order to generate a better animal model of an inflammatory skin condition. The instantly claimed method requires administration APCs intradermally, a method step to which Parker is silent. Therefore, Parker’s teaching wherein CD3+ T cells would have APCs removed is not considered to teach away from coadministration of APCs and CD3+ T cells as Applicant asserts, particularly as coadministration of PBMCs which comprise APCs is taught by Herz.
Response to Applicant’s Affidavit
Applicant asserts and Mr. Kim declares in point number 2 that the claimed invention creates a personalized atopic dermic animal model reflecting a patient’s immune response which was confirmed by infiltration of human T-cells in lymphocytes and antigen-presenting cells (APCs) in non-lymphocytes of injected mice as shown in Example 4 and FIGs 3a-c of the instant disclosure. Applicant asserts in point numbers 3 and 4 that Applicant’s instantly claimed combination of intravenous injection of CD3+ T cells and intradermal injection of APCs provides the allegedly unexpected result of improving the efficiency of reproducing atopic dermatitis symptoms compared to other models. Applicant asserts that additional experiments were performed in order to confirm that the claimed combination of intravenous injection of CD3+ T cells and intradermal injection of APCs allegedly improved the efficiency of reproducing symptoms of atopic dermatitis specifically compared subcutaneous injection of whole PBMCs or intravenous injection of CD3+ T cells alone. In points 5 and 6, Applicant details generation of experimental groups consisting of control/no treatment, T-cell only injection, APC-only injection, and T-cell with APC co-injections with subgroups for each group consisting of no house dust mite treatment and house dust mite treatment and wherein CD3+ T cells from atopic dermatitis patients were injected intravenously and CD3- PBMCs (serving as APCS) were injected intradermally to NSG mice prior to a challenge with house dust mite allergen. Applicant asserts in point 7 that the greatest inflammatory response was induced by the claimed invention of CD3+ T cell intravenous injection and CD3- PBMC intradermal injection as shown in Applicant’s provided images when compared to the model of Parker which teaches injection of CD3+ T cells alone. In points 8-11, Applicant asserts that the combination of CD3+ T cell intravenous injection and CD3- PBMC intradermal injection shows thickening of the epidermis and “immune cell” infiltration in response to house dust mite treatment (Fig. D). Applicant also provides flow cytometry analysis showing increased presence of human CD45+ cells in the blood of subjects receiving donor T-cells and APCs after 4 weeks (Fig G) and showing increased human CD45+, human CD3+, and human APCs in the skin and lymph nodes of subjects receiving donor T-cells and APCs after 4 weeks. Applicant further shows images of increased inflammatory response in skin in response to administration of T-cells and APCs after exposure to house dust mites. Applicant asserts in points 12 and 13 that claimed combination of intravenous injection of CD3+ T cells and intradermal injection of APCs results in the alleged unexpected result of improving the efficiency of reproducing atopic dermatitis symptoms thus providing a patient-tailored dermatitis avatar mouse model when compared to the prior art of Herz and Parker.
Applicant’s arguments and Mr. Kim’s declaration have been considered but are not found persuasive.
Applicant asserts that the claimed combination of intravenous injection of CD3+ T cells and intradermal injection of APCs allegedly improves the efficiency of reproducing symptoms of atopic dermatitis specifically compared subcutaneous injection of whole PBMCs or intravenous injection of CD3+ T cells alone. It is noted that Applicant’s use of “subcutaneous injection” is not consistent with nor is it the same route of administration as the intradermal injection as claimed and as taught in the prior art by Herz. Thus, there is some lack of clarity surrounding the experimental methods used to evaluate the instantly claimed method of generating an avatar mouse which exhibits alleged unexpected results. It is also noted in Example 3 of the instant specification that Applicant indicates the avatar mice of the instant invention could be generated by intravenous injection of CD3+ T cells or whole PBMCs. Applicant’s avatar mice of the working examples in the instant specification appear to be “generated by injecting PBMCs” (Para. [0068]) which is similar to the method of Herz wherein whole PBMCs are injected intraperitoneally in order to generate a humanized atopic dermatitis mouse model. Thus, it appears that the data regarding infiltration of human T-cells and antigen-presenting cells (APCs) shown in the instant specification is from experimental subjects generated by administration of whole PBMCs while the data presented in Applicant’s traversal and Mr. Kim’s declaration is from subjects generated by administration of CD3+ T cells. Additionally, Applicant’s method of generating avatar mice appears to involve intradermal administration of CD3-depleted PBMCs but does not utilize isolated CD14+ monocyte and dendritic cells. Since, rejected claim 1 is directed to either CD3-depleted PBMCs or CD14+ monocyte and dendritic cells, the instant claims are not commensurate in scope with Dr. Kim’s alleged unexpected results.
Furthermore, Applicant does not provide data comparing mouse models generated by intravenous administration of CD3+ T cells as claimed to mouse models generated by intravenous administration of whole PBMCs as previously shown and as detailed in the methods of the prior art. As Herz’s model teaches generation of a humanized mouse model via intraperitoneal injection of whole PBMCs in conjunction of intradermal administration of whole PBMCs, which Herz teaches are necessary for generation of the allergic response, and Parker teaches wherein intravenous injection of CD3+ cells generates a superior mouse model wherein the inflammatory skin is induced in nearly all animals, it appears the differences between the claimed invention as disclosed and the applied prior art are related to either the route of administration of the CD3+ cells/PBMCs or the specific cells which are administered intradermally – whole PBMCs as taught by Herz in comparison with CD3-depleted PBMCs as instantly claimed. In other words, Applicant has not demonstrated that intradermal injection of CD3-depeleted PBMCs actually produces a better result than intradermal injection of whole PBMCs.
With regard to Applicant’s assertion in point 7 that the greatest inflammatory response was induced by the claimed invention of CD3+ T cell intravenous injection and CD3-depleted PBMC intradermal injection when compared to the model of Parker which teaches injection of CD3+ T cells alone, Applicant is reminded that MPEP 2145(IV) states:
“One cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., Inc., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Where a rejection of a claim is based on two or more references, a reply that is limited to what a subset of the applied references teaches or fails to teach, or that fails to address the combined teaching of the applied references may be considered to be an argument that attacks the reference(s) individually.”
As detailed in the previous Office Action, the obviousness rejection was applied based on Herz who teaches a method of generating a mouse model of atopic dermatitis via intraperitoneal and intradermal injections of PBMCs in view of Parker who teaches a method of generating a mouse model of atopic dermatitis via intravenous injection of CD3+ T cells which is superior to those of the prior art. Thus, Parker teaches that use of intravenously administered CD3+ T cells generates the inflammatory skin condition in nearly all animals and Herz teaches the need for an additional intradermal administration of PBMCs in order to generate an allergen response.
Moreover, in regard to the additional data supplied in Applicant’s affidavit dated October 7, 2025, unexpected results are based on objective scientific evidence (See MPEP 2145). It is noted that due to the size and clarity of the images supplied in Applicant’s affidavit, it is difficult to evaluate some of the data. Additionally, because the timeline of Applicant’s experimental data is not clearly stated, it is also difficult to directly compare Applicant’s alleged unexpected results with the closest prior art of Herz and Parker. Applicant provides no details regarding the timeline for administration of CD3+ T cells and CD3-depleted PBMCs to subjects, house dust mite challenge, and evaluation of inflammatory skin responses. However, Herz teaches that intradermal PBMC administration 14 days after intraperitoneal PBMC administration followed by 5 days of challenge with house dust mite allergen results in increased dermal T cell infiltration (Table IV, 2nd line) when compared to control, which appears to be similar to Applicant’s results as stated in point 7. Additionally, Parker teaches wherein mice intravenously injected with CD3+ T cells developed inflammatory skin responses which were present in all animals followed for at least 6 weeks (Col 16, lines 6-7, 9-11, and 14-16) with severity increasing over time (Col. 16, lines 51-53). Thus, one of ordinary skill in the art could expect to demonstrate increasing severity of dermal changes in the animal model of Herz over a longer time period based on the teachings of Parker. Additionally, Parker also teaches dermal infiltration of CD3+ cells in experimental animals (Col. 17, line 35) compared to control animals which is similar to results as shown by Applicant. Thus, it appears that Applicant’s alleged unexpected results are supported by the teachings of the prior art.
With regard to Applicant’s assertion that claimed combination of intravenous injection of CD3+ T cells and intradermal injection of CD3-depleted PBMCs results in the alleged unexpected result of improving the efficiency of reproducing symptoms of atopic dermatitis, it appears, based on the prior art, that Applicant’s claimed mouse model of atopic dermatitis works as expected. Herz teaches generation of mouse model via intraperitoneal and intradermal administration of PBMCs. Parker teaches that administration of intravenous CD3+ cells generates a model which is superior to the prior art and which replicates human symptoms of atopic dermatitis with more fidelity, which is similar to Applicant’s alleged unexpected result with respect to CD3+ T cells. Herz teaches that intradermal injection of PBMCs is required to generate an allergen response to house dust mites and that CD14+ APCs are required for production of the allergen response. Thus, based on the combination of the applied prior art, it appears the method of the instantly claimed invention works as intended and that a skilled artisan would recognize that use of CD3+ cells in generation of the model would increase model efficiency. The differences between the instantly claimed invention and the prior art appear to be in the particular subset of cells given intradermally, specifically whole PBMCs taught by Herz and CD3-depleted PBMCs comprising APCs as instantly disclosed. However, the PBMCs given intradermally as taught by Herz necessarily comprise APCs. As there is no data directly comparing atopic dermatitis symptoms in mice injected intradermally with whole PBMCs to atopic dermatitis symptoms in mice injected intradermally with CD3-depleted PBMCs, there is no way to evaluate the claimed alleged unexpected and improved efficiency compared to the closest prior art of the method as made obvious by the combination of Herz and Parker.
Declaration under 37 CFR 1.132
The declaration under 37 CFR 1.132 filed by Hye Li Kim on 10/07/2025 has been considered and is insufficient to overcome the rejection of instant claims based upon 35 U.S.C 103 as set forth in the last Office action for the following reasons:
It refers only to the system described in the above referenced application and not to the individual claims of the application. As such the declaration does not show that the objective evidence of nonobviousness is commensurate in scope with the claims as it pertains to injection of CD14+ monocyte and dendritic cells as recited in claim 1. See MPEP § 716.
It includes statements which amount to an affirmation that the claimed subject matter functions as it was intended to function as it pertains to injection of CD3-depleted PBMCs as recited in claims 1 and 14. This is not relevant to the issue of nonobviousness of the claimed subject matter and provides no objective evidence thereof. See MPEP § 716.
In view of the foregoing, when all of the evidence is considered, the totality of the rebuttal evidence of nonobviousness fails to outweigh the evidence of obviousness.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/ERIN V PAULUS/Examiner, Art Unit 1631
/ARTHUR S LEONARD/Examiner, Art Unit 1631